acid-phosphatase and Chemical-and-Drug-Induced-Liver-Injury

Sixteen male Suffolk lambs fed a 8 ppm Cu basal diet were randomly assigned to 2 groups: 12 copper-loaded (CL) and 4 controls (C). The CL sheep were drenched initially with 3 mg Cu/kg bw daily for a week. Every week an additional dose of 3 mg Cu/kg bw was included in the drench until signs of copper poisoning appeared; the control sheep were drenched with saline solution. The onset of copper poisoning occurred between 42 and 55 d. Food intake and body weight were recorded daily. Blood samples were collected weekly to measure the activity of the liver enzymes gamma-glutamyltransferase (gammaGT), aspartate aminotransferase (AST), sorbitoll dehydrogenase (SDH) and acid phosphatase (AF). The following changes were significantly recorded in the CL sheep in the weeks or days previous to the hemolytic crisis: higher levels of gammaGT were found on the -28th d increasing slowly but continuously until the hemolytic crisis; SDH fluctuated during the period presenting higher levels on the -28th, -14th and -7th d; AST and AF activities increased from the -14th and -7th d respectively; sharp decreases in the activities of SDH and AF at the hemolytic crisis; lower feed intake and body weight gain from the -7th d; and sheep ceased eating concentrates from the -9th d and became anoretic the day before the hemolytic crisis. Plasma copper concentration increased only the day before the hemolytic crisis. There were no changes in respiratory and heart rates, rectal temperature or rumen movements throughout the pre-hemolytic phase. The higher the amount of cumulative copper drenched, the higher was the gammaGT and AST activities. It was concluded that gammaGT followed by AST are the best enzymes to assess copper-load in sheep during the pre-hemolytic phase. Sheep fed copper-rich diets with high plasma activity of these enzymes, decreased feed consumption and subtle loss of body weight are most likely to present with a hemolytic crisis in a few days.

Topics: Acid Phosphatase; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Copper; Diet; gamma-Glutamyltransferase; L-Iditol 2-Dehydrogenase; Liver; Male; Poisoning; Sheep; Sheep Diseases; Time Factors

The present study is aimed to evaluate the protective effect of ferulic acid (FA) on fluoride-induced oxidative hepatotoxicity in male Wistar rats. Fluoride (25 mg/L) was given orally to induce hepatotoxicity for 12 weeks. Hepatic damage were assessed using status of pathophysiological markers like serum marker enzymes like aspartate transaminase, alanine transaminase, alkaline phosphatase, acid phosphatase, gamma glutamyl transferase, lactate dehydrogenase, bilirubin, lipid profile, total protein content levels, and histopathological studies. Treatment with FA significantly reduced the degree of histological aberrations and rescued lipid peroxidation, as observed from reduced levels of lipid hydroperoxides, nitric oxide, restored levels of enzymic and non-enzymic antioxidants, and total protein content, with a concomitant decline in the levels of marker enzymes and lipid profile in fluoride-induced rats. These results suggest that ferulic acid has the ability to protect fluoride-induced hepatic damage.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; Aspartate Aminotransferases; Bilirubin; Catalase; Chemical and Drug Induced Liver Injury; Coumaric Acids; Fluorides; gamma-Glutamyltransferase; Glutathione; Glutathione Peroxidase; L-Lactate Dehydrogenase; Lipids; Liver; Male; Oxidative Stress; Protective Agents; Rats; Rats, Wistar; Superoxide Dismutase

Microcystins (MC) are frequently present in cyanobacterial blooms in rivers and lakes, increasing the risk of toxicity to both animals and humans. There more than eighty reported microcystins, and the present study was undertaken to determine whether MC-LR and MC-RR can induce different enzyme alterations and histopathological changes in tilapia fish (Oreochromis sp.) exposed to a single intraperitoneal (i.p.) injection of the pure standards (MC-LR and MC-RR) at a dose of 500 mug/kg; the tilapia fish were then observed for seven days. The two MC variants caused significant changes in the activities of acid and alkaline phosphatases (ACP and ALP) in vital organs, showing a different response pattern. The livers and kidneys of fish injected with MC-LR were particularly affected. MC-RR induced a very pronounced increase of ACP in the kidney and a significant increase of ALP in the liver. Both MC variants caused pathological lesions in hepatic tissues, such as megalocytosis, necrotic process, and microvesicular steatosis, particularly in fish treated with MC-LR, and degenerative renal changes, glomerulopathy, were more severe in tilapias exposed to MC-RR. In addition, both microcystins also caused significant myopathy in the heart. In contrast, the gills did not show any change in enzyme activity or histopathological injury.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Bacterial Toxins; Chemical and Drug Induced Liver Injury; Cichlids; Gills; Heart; Injections, Intraperitoneal; Kidney; Kidney Diseases; Liver; Liver Diseases; Microcystins; Myocardium; Organ Size

The present study has been conducted to evaluate the curative effect of propolis extract, a honey bee-hive product, against acetaminophen (APAP) induced oxidative stress and dysfunction in liver and kidney. Animals were challenged with APAP (2 g/kg, p.o.) followed by treatment of propolis extract (100 and 200 mg/kg, p.o.) once only after 24 h. Release of transaminases, alkaline phosphatase, lactate dehydrogenase, and serum bilirubin were increased, whereas hemoglobin and blood sugar were decreased after APAP administration. Antioxidant status in both the liver and kidney tissues were estimated by determining the glutathione, malondialdehyde content and activities of the CYP enzymes, which showed significant alterations after APAP intoxication. In addition, activities of adenosine triphosphatase, acid phosphatase, alkaline phosphatase, and major cell contents (total protein, glycogen and cholesterol) were also altered due to APAP poisoning. Propolis extract successfully reversed the alterations of these biochemical variables at higher dose. Improvements in hepatorenal histoarchitecture were also consistent with biochemical observations. The results indicated that ethanolic extract of propolis has ability to reverse APAP-induced hepatorenal biochemical and histopathological alterations probably by increasing the antioxidative defense activities due to various phenolic compounds present in it.

Topics: Acetaminophen; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Antioxidants; Bilirubin; Blood Glucose; Chemical and Drug Induced Liver Injury; Cholesterol; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Female; Glutathione; Glycogen; Hemoglobins; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Liver; Liver Diseases; Malondialdehyde; Oxidative Stress; Propolis; Rats; Rats, Sprague-Dawley; Silymarin; Transaminases

Lead acetate (300 mg Pb/L) and/or cadmium acetate (10mg Cd/L) in blood and liver were administrated as drinking water to pregnant Wistar rats from day 1 of pregnancy to parturition (day 0) or until weaning (day 21), to investigate the toxic effects in blood and in the liver. Both metals produced mycrocitic anaemia in the pups as well as oxidative damage in the liver, as suggested by the significant increase in TBARS production and the high catalase activity. Moreover, intense alkaline and acid phosphatase activity, used as biomarkers of liver adaptation to damaging factors, was observed. In addition, the toxikinetics are different for Pb and Cd: while Cd is a hepatotoxic from day 0, Pb is not until day 21. Finally, simultaneous perinatal administration of both metals seems to protect, at least, in the liver TBARS production against the toxicity produced by Cd or Pb separately.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Animals, Newborn; Cadmium; Cadmium Poisoning; Catalase; Chemical and Drug Induced Liver Injury; Drug Combinations; Female; Lead; Lead Poisoning; Liver Diseases; Organ Size; Oxidative Stress; Pregnancy; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances

This study was designed to investigate the hepatotoxicity of ranitidine treatment in dose levels of 10, 30, and 50 mg/kg b.wt. for 3 weeks period in male rats. The results showed some adverse changes in rats treated with either 10 or 30 mg/kg. Treatment with dose of 50 mg/kg produced marked increase in the activity of both acid phosphatase in liver and aspartate aminotransferase in serum and liver, with a tendency for increase in serum alanine aminotransferase activity. Also, a significant decrease in the serum activity of both amylase and alkaline phosphatase was noted. Microscopic examination of livers of the same animals revealed absence of some hepatic cells, pyknotic nuclei, dilatation of blood sinusoids, binucleated cells, and infiltration of lymphocytes. These biochemical and histological changes indicate that ranitidine when given chronically in high dose could produce hepatotoxicity in rats.

Topics: Acid Phosphatase; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Dose-Response Relationship, Drug; Histamine H2 Antagonists; Humans; Liver; Male; Ranitidine; Rats

We investigated the relationship between DNA degradation and lysosome activity (loss of lysosomal integrity) in necrotic cell death induced by carbon tetrachloride (CCl4) and dimethylnitrosamine (DMN): coagulation necrosis and hemorrhagic necrosis, respectively. TdT-mediated dUTP-biotin nick end-labeling (TUNEL) and enzyme histochemistry for acid phosphatase were performed in both models and results were analyzed by light microscopy, electron microscopy, and confocal laser scanning microscopy (CLSM). In the CCl(4)-injected liver, TUNEL staining was closely associated with release of lysosomal enzymes into the cytoplasm, and intranuclear deposition of lysosomal enzymes took place at an early stage of subcellular damage. In the DMN-injected liver, TUNEL-positive nuclei tended to have well-preserved lysosomes and centrally localized TUNEL signals. It was assumed that acute hepatocellular damage in the CCl4-injected liver would be characterized by necrotic cell death with lysosome activation and that damage in the DMN-injected liver would be necrotic cell death without lysosome activation. In the DMN-injected liver, DNA degradation may be selectively induced in the nuclear center, in which heterochromatin (including inactive chromatin) is believed to be a target. We concluded that necrotic cell death, i.e., DNA degradation, would be at least divided into two types, with/without association with lysosome activation, represented by necrotic cell death in the CCl4-injected liver and that in the DMN-injected liver.

Topics: Acid Phosphatase; Acute Disease; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Dimethylnitrosamine; In Situ Nick-End Labeling; Lysosomes; Male; Microscopy, Confocal; Microscopy, Electron; Necrosis; Rats; Rats, Wistar

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Antibiotics, Antineoplastic; Ascorbic Acid; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Confidence Intervals; Daunorubicin; Liver Diseases; Male; Rats; Rats, Wistar; Vitamin E

The preventive effects of a traditional Chinese medicine Sho-saiko-to (Kampo prescription, TJ-9) were determined from oxygen toxicity and membrane damage in liver during endotoxemia. The liver lipid peroxide level and xanthine oxidase activity 18 h after administration of endotoxin (6 mg/kg, i.p.) to TJ-9 (500 mg/kg/d, p.o.)-pretreated mice were markedly lower than that in endotoxin-treated mice, whereas the administration of TJ-9 significantly increased superoxide dismutase and glutathione peroxide activities in liver of endotoxin-injected mice. In the mice pretreated with a TJ-9, the levels of alpha-tocopherol and nonprotein SH in liver tissue 18 h after endotoxin injection were markedly increased as compared to those in endotoxin-treated mice. Leakages of acid phosphatase and lactate dehydrogenase isozyme in serum were markedly lower in endotoxin-TJ-9-treated mice than those in mice given endotoxin. The administration of TJ-9 clearly prevented the membrane protein damage arising from endotoxin challenge. Kampo prescription Sho-saiko-to thus appears to protect the liver plasma membrane from injury by free radicals which occur in a tissue ischemic state during endotoxemia.

Topics: Acid Phosphatase; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Membrane; Chemical and Drug Induced Liver Injury; Drugs, Chinese Herbal; Electrophoresis, Polyacrylamide Gel; Free Radical Scavengers; In Vitro Techniques; Isoenzymes; L-Lactate Dehydrogenase; Lipid Peroxides; Liver; Male; Mice; Mice, Inbred Strains; Oxygen; Shock, Septic; Sulfhydryl Compounds; Vitamin E

To determine whether lysosomal lipid composition is altered in hepatic necrosis, we studied this parameter in thioacetamide-induced necrosis and in its regenerating stage as well as in the recovery of thioacetamide-induced injury. Results showed that in liver necrosis there is an increase in the protein and phospholipid lysosomal contents. This effect may be related to an increased number of lysosomes. These organelles also suffered a decrease in cholesterol content. When liver necrosis was recovered either pharmacologically or spontaneously all three parameters recovered their normal values. These results suggest that lysosomes and their lipid composition play a role in progression of hepatic necrosis.

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Cholesterol; Lipid Metabolism; Lysosomes; Male; Membranes; Necrosis; Rats; Rats, Wistar; S-Adenosylmethionine; Thioacetamide

Lantadene C (22 beta-2-methylbutanoyloxy-3-oxoolean-12-en-28-oic acid) isolated from the leaves of the hepatotoxic plant Lantana camara var. aculeata (Red) has been found to be identical with dihydrolantadene A reported earlier. Molecular structure of lantadene C has been deduced from single crystal X-ray diffraction analysis. It resembles lantadene A in the pentacyclic portion of the molecule but differs in the side chain region. Atom C-34 is cis to C-35 in lantadene C but is trans in lantadene A. Semisynthetic lantadene C was prepared by catalytic hydrogenation of lantadene A. Lantadene C was obtained in two forms, I and II. Form I was crystalline while form II was amorphous. Unlike lantadene A, both form I and II of lantadene C elicited strong hepatotoxic response in guinea pigs associated with decrease in fecal output, feed intake, hepatomegaly, hepatic injury at the cellular and subcellular level, increase in plasma bilirubin, and acid phosphatase activity. All the clinical signs, hepatic lesions, and changes in blood plasma typified lantana toxicity. This is the first report on the hepatoxicity of lantadene C. The interrelation of molecular structure and biological activity of lantadene A and C has been discussed.

Topics: Acid Phosphatase; Animals; Bilirubin; Chemical and Drug Induced Liver Injury; Crystallization; Guinea Pigs; Liver; Liver Diseases; Male; Molecular Structure; Oleanolic Acid; Plant Extracts; Stereoisomerism; Toxins, Biological; X-Ray Diffraction

The alterations of haematological parameters in albino rats were studied after oral administration of an aqueous extract of silken styles of corn (Zea maize Linn.) at 50, 100 and 150 mg kg-1 daily for 21 days. The following haematological values were significantly reduced on the 7th and 21st day following extract administration: haemoglobin (Hb), red blood corpuscles (RBC), clotting time (CT), mean corpuscular volume (MCV), haematocrit (Ht), serum glucose, blood urea nitrogen (BUN), cholesterol, aspartate transaminase (AST), alanine transaminase (ALT), calcium, total protein, total albumin and total acid phosphatase; and white blood corpuscles (WBC), mean corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), alkaline phosphatase and creatinine increased. The remaining parameters were not significantly affected, except body weight parameters at the two highest doses. The results emphasize that the biochemical changes caused through aqueous extract of silken styles of corn (Zea maize Linn.) are not significantly toxic at low and medium doses (50 and 100 mg kg-1).

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Blood Coagulation; Blood Glucose; Blood Proteins; Blood Sedimentation; Blood Urea Nitrogen; Blood Volume; Body Weight; Calcium; Chemical and Drug Induced Liver Injury; Cholesterol; Dose-Response Relationship, Drug; Hematocrit; Hematologic Diseases; Hemoglobins; Leukocytes; Male; Plant Extracts; Rats; Serum Albumin; Zea mays

Liver cytotoxic alterations of adult medaka (Oryzias latipes) following short-term bath exposure (48 hr) to 500 mg/L diethylnitrosamine (DEN) were studied (days 3-21) by electron microscopy and cytochemistry. Control medaka displayed hepatic sexual dimorphism as described for other sexually active fish. Following DEN exposure, decreased glycogen stores with loss of cellular compartmentation obscured sexual dimorphism. A spectrum of organelle alterations, previously not reported in livers of fish, was seen. Early changes in hepatocytes included: nuclear lipid inclusions, nucleolar changes, decreased amounts of granular endoplasmic reticulum (GER), increased fractionation and steatosis of GER, proliferation of smooth ER and lysosomes, reduction in number and content of particulate lipoproteins and vitellogenin in Golgi vesicles, and reduction in number and staining intensity of peroxisomes. At day 14 and/or 21, partial to complete reversal of the above alterations indicated hepatic recovery, and fewer necrotic cells were seen at day 21 versus day 14. Lesions that did not resolve during this study were altered mitochondria and areas of spongiosis hepatis that developed at day 8 and continued to increase throughout the study. Infiltration of lymphocytes, granulocytes, and large numbers of macrophages were late changes. The description, timing, and duration of lesions are of value for consideration as biomarkers of exposure and effect in aquatic toxicology.

Topics: Acid Phosphatase; Animals; Carcinogenicity Tests; Catalase; Chemical and Drug Induced Liver Injury; Diethylnitrosamine; Female; Histocytochemistry; Liver; Liver Glycogen; Male; Microscopy, Electron; Mitochondria, Liver; Oryzias

In the experiments on Wistar rats we showed that administration of ulcerogenic drugs (cinchophen, acetylsalicylic acid, butadione, indomethacin etc.) produced the alterations of free activity of lysosomal enzymes in the homogenates of ulcerated stomach, presumably the significant elevation of the activity of cathepsins (more often cathepsin with optimum of activity at pH 5.5) and the significant reduction of free activity of acid nucleases (more often of DNA-ase). The alterations of free activity of lysosomal enzymes were as in cases with gastric ulcerations as in cases with unaffected stomach.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride; Cathepsins; Chemical and Drug Induced Liver Injury; gamma-Glutamyltransferase; Liver; Lysosomes; Male; Phenylbutazone; Quinolines; Rats; Rats, Inbred Strains; Transaminases

The biochemical basis of the hepatitis-like liver injury produced by D(+)-galactosamine in rats is well-established and is linked to depletion of uridine nucleotides within parenchymal cells. However, the prominent inflammatory response that accompanies this lesion in vivo has been largely overlooked as a component of the hepatic damage. This study examines the cellular components of the inflammatory infiltrate of galactosamine-induced liver injury over time using histochemical and ultrastructural techniques. By 12 h after toxin administration, the infiltrate consisted largely of neutrophils and recently-mobilized monocytes. By 24 to 48 h after the toxin, when hepatocellular necrosis was maximal, few neutrophils were found in the infiltrate. At these times, the infiltrate consisted almost exclusively of large phagocytic cells, histochemically and morphologically consistent with active tissue macrophages apparently derived from circulating monocytes. The extent of the inflammatory response to this experimental hepatotoxin suggests that effects on the generation and development of the inflammatory response should be considered for treatments reported to alter the intrinsic hepatotoxicity of galactosamine.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Galactosamine; Inflammation; Lectins; Liver; Male; Microscopy, Electron; Monocytes; Neutrophils; Peanut Agglutinin; Rats; Rats, Inbred Strains

CB3717 is a quinazoline antifolate whose cytotoxic activity is mediated by inhibition of thymidylate synthase (TS). A phase I clinical trial commenced in September 1981 and 99 patients have received 296 treatments. Doses were dissolved in 0.15 mol/L NaHCO3 (pH 9.0) at a concentration of 4 mg/mL infused over one hour or in a total volume of 1 L infused over 12 hours. Doses were repeated every 3 weeks. The starting dose of 140 mg/m2 was escalated to 600 mg/m2. Renal toxicity, detected by a decrease in the 51Cr EDTA clearance, was dose-related and occurred in seven of ten patients receiving greater than 450 mg/m2. Reversible hepatic toxicity often associated with malaise occurred in 223 of 288 assessable courses (77%). Fifty-nine courses (20%) were associated with increases in alanine transaminase (ALT) levels to greater than 2.5 times the upper limit of the normal laboratory range. Increases in alkaline phosphatase levels also occurred, but were less marked. The severity and prevalence of these elevations were unaffected by the duration of the infusion. A self-limiting rash appeared in 12 patients and a radiation recall reaction was seen in two. Leukopenia developed in 17 patients (WBC less than 3 X 10(9)/L), and thrombocytopenia occurred in six patients (platelets less than 100 X 10(9)/L). The mean leucocyte nadir occurred on day 10 and was followed by recovery at 11 to 19 days. Neither the incidence nor the severity of any of these latter toxicities was dose related. The maximum tolerated dose was in the region of 600 mg/m2 with renal toxicity being dose limiting, although the inter-patient variation did not allow a precise definition. Seventy-six patients were evaluable for response. Responses occurred at doses greater than or equal to 200 mg/m2 and were ovary, one complete response (CR), one partial response (PR), seven minor responses (MR) in 30 cases; breast, two PRs and one MR in eight cases; adenocarcinoma of the lung, one MR in 5 cases; mesothelioma, one PR in five cases; and colon, two MRs in four cases. CB3717 has activity in heavily pretreated patients. The recommended phase II dose for good-risk patients is 400 mg/m2 using the one-hour infusion schedule of administration.

Topics: Acetylglucosaminidase; Acid Phosphatase; Alanine Transaminase; Antineoplastic Agents; Chemical and Drug Induced Liver Injury; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Evaluation; Folic Acid; Folic Acid Antagonists; Glomerular Filtration Rate; Hematologic Diseases; Hyperbilirubinemia; Kidney Diseases; Leucyl Aminopeptidase; Neoplasms; Quinazolines; Skin Diseases; Thymidylate Synthase

Topics: Acetaminophen; Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Glucose-6-Phosphatase; Liver Diseases; Male; Microsomes, Liver; Phenobarbital; Rats; Rats, Inbred Strains

Topics: Acid Phosphatase; Animals; Arginase; Arginine; Carbon Tetrachloride Poisoning; Cathepsin D; Cathepsins; Chemical and Drug Induced Liver Injury; Liver; Lysosomes; Male; Ornithine Carbamoyltransferase; Rats; Rats, Inbred Strains; Spleen; Time Factors

The development of hepatitis, induced in 48 rats by the administration of galactosamine (GalN) in varying doses, was studied with the use of substrate and enzyme histochemical techniques. The so-called atypical glycogen, which is at first highly resistant to diastase, was shown to be digestible after deamination. The increasing accumulation of atypical glycogen during the course of GalN-hepatitis conceals the loss of normal glycogen when the PAS-reaction is used. Nevertheless glycogenolysis could also be demonstrated by the increasing activity of phosphorylase. The acid phosphatase activity was progressively diminished, which was interpreted as signifying early lysosomal damage. G6Pase activity remained nearly constant but SDH showed a decrease in activity after 12 h. These histochemical results are considered to provide deeper insight into the pathological mechanism of GalN-hepatitis.

Topics: Acid Phosphatase; Animals; Carbohydrate Metabolism; Chemical and Drug Induced Liver Injury; Galactosamine; Glucose-6-Phosphatase; Glycogen; Liver; Male; Phosphorylases; Rats; Succinate Dehydrogenase

Topics: Acetamides; Acid Phosphatase; Alkaline Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Fructose-Bisphosphate Aldolase; Glucuronidase; Isoenzymes; Liver; Oxidoreductases; Rats; Thioacetamide; Transaminases

Role of lipid peroxidation on lysosomal instability in liver tissue was investiaged in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet. Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well as beta-glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet. Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, beta-glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction. It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further to cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Female; Galactosamine; Glucuronidase; Lipid Metabolism; Liver; Lysosomes; Oxidation-Reduction; Rats; Vitamin E; Vitamin E Deficiency

Lysosome are subcellular particles in which several acid hydrolases of various specificities are localized. The role of lysosome in cellular physiology and pathology has drawn considerable recent attention by several groups of investigators. The purpose of this study was to investigate the activities of lysosomal enzymes--acid phosphatase, beta-glucuronidase, N-acetyl-beta-glucosaminidase--in hepatic disorders. 1) The serum levels of beta-glucuronidase and N-acetyl-beta-glucosaminidase were significantly elevated in patients with diseases of the hepatobiliary system. 2) N-acetyl-beta-glucosaminidase activity in urine specimens from patients with diseases of the hepatobiliary system was found to be significantly higher than in urine specimens from normal adults. 3) Male albino rats of 150 approximately 200 g body weight were used. CCl4 was injected intraperitoneally (dose 0.1 ml of CCl4 per 100 g body weight twice a week for eight weeks). The free activities of lysosomal enzyme were increased and high free/total activity ratios were found in the liver lysosomal fraction of CCl4 intoxicated rats. The results of these experiment indicated that the membranes of lysosome were more permeable to their enzymes, and the release of these enzymes were found in the experimental fatty liver by CCl4. 4) Corticosteroids and chloroquine stabilized rat liver lysosome in vitro from the labilizing influence of incubation at 37 degrees C. 5) The administration of chloroquine to CCl4 intoxicated rats did not cause any well-expressed stabilization of lysosomes. 6) When alpha-Tocopherol was administrated to CCl4 intoxicated rats, the decrease of bound activity and increase of free activity in lysosomal fraction, and increase of acid hydrolases, GOT and GPT in serum were inhibited.

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Chloroquine; Glucuronidase; Hexosaminidases; Humans; Jaundice; Liver Diseases; Liver Neoplasms; Lysosomes; Male; Rats; Vitamin E

The effects of acute and chronic administration of D-Galactosamine (GalN), Ethanol and Phenobarbital were investigated on the activities of lysosomal enzymes, i.e.; acid phosphatase, beta-glucuronidase and n-acetyl-beta-glucosaminidase, and others such as gamma-GTP and adenosine triphosphatase. The histochemical distribution of gamma-GTP in the liver was also studied on biopsy specimens from patients with chronic hepatitis, and gamma-GTP levels in the serum of patients receiving drugs inductable of hepatic microsomal enzymes. 1) After a single intraperitoneal injection of GalN, the lysosomal enzyme activities were lowered in the necrotic areas, but raised in the perinecrotic areas, the proliferative Kupffer cells and intra- and/or extra-cellular eosine bodies. 2) gamma-GTP activities in rat liver after chronic administration of GalN were markedly increased in bile canalicular membrane of periportal parenchymal cells, the epithelium of bile duct and ductules, and som inflammatory cells of portal fields. Levels of serum gamma-GTP were also elevated. On histochemical studies with biopsy specimens from patients with chronic active hepatitis showing elevated gamma-GTP activity, the activity was revealed a similar localization to GalN-treated rats. These data suggested that the increased activities might be reflected on the active stage in chronic hepatitis. 3) Chronic ethanol treatment in rats induced clearly-stained lysosomes varied in size, especially large-sized. The activities of hepatic gamma-GTP were slightly increased in the bile canalicular membrane of periportal parenchymal cells and the epithelium of proliferative bile ductules. 4) It has been shown by histochemical and biochemical techniques that hepatic gamma-GTP activity was increased after phenobarbital administration in rats. A significant rise in serum gamma-GTP was observed in patients on long-term treatment with anti-epileptic drugs. These data indicated that the increased activities of serum gamma-GTP might be accompanied with induction of hepatic microsomal drug-metabolizing enzymes.

Topics: Acetylglucosaminidase; Acid Phosphatase; Adenosine Triphosphatases; Alcoholism; Animals; Anticonvulsants; Chemical and Drug Induced Liver Injury; Ethanol; Galactosamine; gamma-Glutamyltransferase; Glucuronidase; Histocytochemistry; Humans; Liver; Liver Diseases; Lysosomes; Male; Phenobarbital; Rats

Topics: Acetylglucosaminidase; Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hexosaminidases; Lysosomes; Rats

The effect of a single injection of lysosomotropic agent--Triton WR-1339 on the properties of the rat liver lysosomes and the course of pathological process during chronic toxic hepatitis were studied. Triton WR-1339 administration was followed by a more rapid restoration of the liver structure and function. A possible mechanism of the favourable effect of Triton WR-1339 is discussed.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Cell Nucleolus; Cell Nucleus; Chemical and Drug Induced Liver Injury; Chronic Disease; Liver; Lysosomes; Male; Polyethylene Glycols; Rats; Ribonucleases; Sulfobromophthalein

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Endotoxins; Injections, Intraperitoneal; Liver; Liver Diseases; Male; Necrosis; Rats

The hepatoprotective action of Silymarin was studied in 65 male Wistar rats, prior to and following D-galactosamine intoxication. There was a marked reduction in the histological and ultrastructural changes in the nucleolus, nuclear membrane, mitochondria, granular and agranular endoplasmic reticulum and lysosomes of the liver cell and also in the Kupffer stellate cells. The reduction in glycogen and RNA loss was determined biochemically. The activities of many enzymes were kept constant (oxidoreductases, NADH2 diaphorase, G-6-phosphatase, Mg++ and K+/Na+-dependent ATPases, acid phosphatases).

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Cell Membrane; Chemical and Drug Induced Liver Injury; Drug Evaluation; Flavonoids; Galactosamine; Glucose-6-Phosphatase; Liver; Liver Glycogen; Male; Mitochondria, Liver; Nucleic Acids; Oxidoreductases; Rats; Silymarin

In the cholestatic condition of many different aetiologies a common pathologic picture is found. It is characterized by the presence of pigmented "plugs" and cytoplasmatic "masses" in the centrolobular region. Dubin has tried to interpret this on purely hydrostatic ground but this is not a very likely explanation. We tried to comprove this hypothesis studying the interference of a previous, or concomitant, centrolobular alteration in the distribution, morphology and intensity of cholestatic lesions: terminal choledochus ligatures were performed in animals intoxicated with carbon tetrachloride, a substance that damages predominantly the centrolobular region. In 6 dogs, terminal choledochus ligature was associated with carbon tetrachloride intoxication. A histological examination of the liver showed that the degree of centrolobular cholestasis was in the inverse ration of hepatocytic damage intensity. This fact does not conform with Dubin's hypothesis.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cholestasis; Dogs; Liver; Male

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Chlorpromazine; Liver; Lysosomes; Male; Rats

An increased stability of liver lysosomes and mitochondria of burned, dehydrated and tumour-bearing rats has been found in the present investigations. Using biochemical criteria we were able to show that the membranes of liver subcellular particles of these animals become more resistent to the labilizing action of CCl4. The latter effect was confirmed by electron microscopic data. The tumour growth, dehydration and burning of rats as well as sleep deprivation, overheating, lanthanum and ruthenium red have been shown to cause changes in the activity of some enzyme-systems located in endoplasmic reticulum. The protective action of these chemical, pathological and stress factors against CCl4 produced damage to the cell organelles studied is discussed in relation to the activity of the drug metabolizing pathways; biochemical (modifying of some enzyme activity) as well as pharmacological (duration of hexobarbital sleep) data were used as criteria for the activity of these pathways.

Topics: Acid Phosphatase; Aniline Hydroxylase; Animals; Burns; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Dehydration; Endoplasmic Reticulum; Female; Liver; Liver Diseases; Lysosomes; Male; Microscopy, Electron; Mitochondria, Liver; Oxygen Consumption; Rats; Stress, Physiological

A histochemical study of plasma-membrane associated enzymes in rat liver demonstrated a significant lesion 3 days after a single oral dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin). The complete loss of canalicular ATPase reaction in the parenchymal cells of the centrilobular zone remained the prominent feature of the liver throughout the 6-wk period studied. Involvement of the periportal and midzonal regions occurred in moribund animals and improvement in the health of two surviving animals at 9 mth was associated with a normal distribution of ATPase in the liver. Qualitative changes in 5-nucleotidase and acid phosphatase were secondary to the parenchymal cell damage. This lesion supports the morphological evidence, reported previously, that the parenchymal cell plasma-membrane is a specific subcellular site of the toxic action of dioxin.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Cell Membrane; Chemical and Drug Induced Liver Injury; Dioxins; Female; Histocytochemistry; Liver; Liver Diseases; Nucleotidases; Polychlorinated Dibenzodioxins; Rats; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Chemical and Drug Induced Liver Injury; Deoxyribonucleases; Furaldehyde; Liver; Male; Rats; Succinate Dehydrogenase

Male Wistar rats were given 50 mug of aflatoxin B1 twice a week for 4 weeks, and thereafter 75 mug twice a week for 10 weeks. Their livers were investigated histologically and histochemically for glycogen, RNA, fat, alkaline and acid phosphatases, adenosine triphosphatase, 5'-nucleotidase, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, succinic dehydrogenase, and alkaline and acid nucleases. No significant lesions occurred before 15 weeks. During this period, the liver was histochemically unchanged except for a periportal decrease of alkaline phosphatase and adenosine triphosphatase. Scattered hepatocytes with a strong glucose-6-phosphatase activity appeared. These changes represent toxic effects of aflatoxin B1 and are irrelevant to carcinogenesis. From 15 weeks onward, three types of liver cell hyperplastic foci and nodules developed. Histologically, and with respect to glycogen, fat, and RNA content, only two of these types were considered as potential precursors of hepatocarcinomas. However, all types exhibited a decrease or absence of the enzymes studied. Both histological and histochemical changes stressed the complex heterogeneity existing between and within hepatic foci and nodules. From 11 months on, hepatocarcinomas developed. The tumors disclosed similar histochemical changes. This similarity further supports the "precarcinomatous" nature of hyperplastic foci and nodules. It appears that focal changes in surface as well as in cytoplasmic and nuclear enzymes are intimately and very early linked to the carcinogenic process. Whether they are fundamental or only represent an epiphenomenon remains unclear.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Aflatoxins; Alkaline Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Glucose-6-Phosphatase; Glucosephosphate Dehydrogenase; Glycogen; Lipid Metabolism; Liver Neoplasms; Male; Neoplasms, Experimental; Nucleotidases; Precancerous Conditions; Rats; RNA, Neoplasm; Succinate Dehydrogenase; Time Factors

In the course of liver injury induced by CCl4 in rats the change of the endoplasmic reticulum takes 5 hours and that of the lysosomal membrane, 18 hours to develop. The latter change precedes hepatocellular necrosis. Elevation of plasma free fatty acids and fatty infiltration of the liver can be observed at 3 hours after CCl4 administration. The maximum of fatty infiltration, hepatocellular necrosis and the highest degree of lysosomal damage develop at the same time. Since CCl4 is eliminated in a few hours, it must initiate a cellular process which then leads to lysosomal membrane damage and hepatocellular necrosis.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cytosol; Fatty Acids, Nonesterified; Female; Glucose-6-Phosphatase; Lipid Metabolism; Liver; Liver Diseases; Lysosomes; Male; Necrosis; Rats; Time Factors

Preliminary administration of triton WR 1339 produced a favourable effect on the course of chronic toxic hepatitis. This was expressed in a reduction of necrotic zones, a delay in development of connective tissue and in improvement of the functional capacity of the liver. Lysosomes of the liver of animals subjected to the action of CCl-4 under conditions of preliminary administration of a detergent were more stable to the injurious actions in vitro.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Chronic Disease; Kupffer Cells; Liver; Lysosomes; Male; Necrosis; Polyethylene Glycols; Quaternary Ammonium Compounds; Rats; Rats, Inbred Strains

Some sympatholytic agents have been tested for the ability to counteract either the hepatotoxic or the lethal effect of A. phalloides in rats. Propranolol displayed a marked preventive action on the liver damage induced by the poison, but only a moderate influence on the lethality. Reserpine was uneffective in terms of liver derangement, but exerted some protection against the general toxic effect of A. phalloides. Other alpha- or beta-adrenolytic compounds failed to afford any significant protection with respect to both liver injury and lethality. It is suggested that propranolol might interfere with transport or binding of phallotoxins to the liver.

Topics: Acid Phosphatase; Animals; Butoxamine; Catecholamines; Chemical and Drug Induced Liver Injury; Epinephrine; Male; Mushroom Poisoning; Norepinephrine; Phentolamine; Practolol; Propranolol; Rats; Reserpine; Sympatholytics

Rats were killed at various time-intervals up to 48 hr after a single large dose of paracetamol (3 g per kg) and their livers examined by light and electron microscopy. In general, this revealed glycogen depletion, loss of ribosomes, and cytoplasmic matrix swelling commencing 3-6 hr after administration which in centrilobular hepatocytes progressed to frank coagulative necrosis at 12-24 hr. Midzonal cells showed more prominent aqueous swelling with besiculation of the endoplasmic reticulum, and in some cells, gross hydropic vacuolation.

Topics: Acetaminophen; Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Endoplasmic Reticulum; Histocytochemistry; Liver; Liver Diseases; Lysosomes; Macrophages; Male; Microscopy, Electron; Necrosis; Rats; Rats, Inbred Strains; Ribosomes; Succinate Dehydrogenase; Time Factors; Vacuoles

A study was made of permeability of the lysosome membranes and subcellular distribution of acid hydrolases in chronic hepatitis caused by CCl4 inhalation and during the restoration of the liver after injury. No normalization of the indices under study occurred during the period of up to 14 days after the last CCl4 inhalation: changes in the stability of the lysosome membran persisted and redistribution of acid hydrolases was noted. This redistribution was associated with both the processes of injury and restoration of the liver.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Cell Membrane; Chemical and Drug Induced Liver Injury; Chronic Disease; Environmental Exposure; Liver; Liver Regeneration; Lysosomes; Male; Proteins; Rats; Ribonucleases; Subcellular Fractions; Time Factors

Changes occurring in the lysosome population were assessed by the results of studies of intracellular distribution of the marker lysosome enzymes--acid phosphatase and acid RNAase. An acute (pure CCl4-0.15 ml per 100 g of weight into the stomach) and chronic (inhalation poisoning after Rabinovici and Wiener) toxic hepatitis was accompanied by an increase in the specific activity of the enzymes in the fraction of heavy mitochondria, this pointing to the change in the sedimentation properties of the lysosomes. An increase in "nonprecipitable" activity of the acid RNA-ase in chronic toxic hepatitis served as the sign of injury of the lysosome membranes.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Cell Nucleus; Chemical and Drug Induced Liver Injury; Endonucleases; Liver; Lysosomes; Male; Microsomes, Liver; Mitochondria, Liver; Phosphates; Rats; Ribonucleases

Topics: Acid Phosphatase; Alcohols; Animals; Cell Nucleus; Centrifugation, Density Gradient; Chemical and Drug Induced Liver Injury; Deoxyribonucleases; Glucose-6-Phosphatase; Liver; Male; Necrosis; Rats; Ribonucleases; Succinate Dehydrogenase; Vacuoles

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carbon Disulfide; Cell Membrane; Chemical and Drug Induced Liver Injury; Edema; Endoplasmic Reticulum; Glucose-6-Phosphatase; Histocytochemistry; Liver; Liver Diseases; Male; Mixed Function Oxygenases; Nucleotidases; Phenobarbital; Rats; Starvation; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Esterases; Female; Glycogen; Histocytochemistry; L-Lactate Dehydrogenase; Lanthanum; Liver; Liver Diseases; Malate Dehydrogenase; Male; Phosphorylase Kinase; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Aminobenzoates; Analgesics; Animals; Antipyrine; Carbon Tetrachloride Poisoning; Cell Membrane; Chemical and Drug Induced Liver Injury; Liver; Lysosomes; Male; Phenylbutazone; Pyrazoles; Rats; Ribonucleases; Stearic Acids

Topics: Acid Phosphatase; Animals; Body Temperature; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cordotomy; Fatty Acids, Nonesterified; Female; Liver; Male; Rats; Spinal Cord; Time Factors

Topics: Acid Phosphatase; Alkaloids; Ammonium Sulfate; Animals; Chemical and Drug Induced Liver Injury; Dithiothreitol; DNA-Directed RNA Polymerases; Glucuronidase; Hemolysis; Liver; Liver Diseases; Organ Size; Peptides; Perfusion; Potassium; Rats; Temperature

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carbon Disulfide; Chemical and Drug Induced Liver Injury; Histocytochemistry; Liver; Liver Diseases; Potassium; Rats; Sodium; Water

Topics: Acid Phosphatase; Adipose Tissue; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Fatty Acids, Nonesterified; Female; Glucose-6-Phosphatase; Lipid Metabolism; Lipid Mobilization; Liver; Lysosomes; Male; Propranolol; Rats

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Berylliosis; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Liver; Lysosomes; Male; Rats; Time Factors

Topics: Acid Phosphatase; Administration, Oral; Animal Feed; Animals; Blood Proteins; Bursa of Fabricius; Capillary Fragility; Chemical and Drug Induced Liver Injury; Chickens; Fusarium; Hematoma; Hemoglobins; Lipids; Liver; Liver Diseases; Mycotoxins; Organ Size; Pancreas; Poultry Diseases; Spleen

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Esterases; Histocytochemistry; Liver; Malathion; Male; Rats

Topics: Acid Phosphatase; Aminohydrolases; Ammonia-Lyases; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Glucuronidase; Histidine Ammonia-Lyase; Hydrolases; Liver; Male; Rats; Spironolactone

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cholestasis; Cholinesterases; Clinical Enzyme Tests; Diagnosis, Differential; Ethionine; Fatty Liver; Fructose-Bisphosphate Aldolase; Fructosephosphates; Necrosis; Phenobarbital; Proadifen; Rats; Thioacetamide

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Cell Membrane Permeability; Chemical and Drug Induced Liver Injury; Liver; Lysosomes; Male; Rats; Ribonucleases; Time Factors

Topics: Acid Phosphatase; Acute Disease; Adenosine Triphosphatases; Adult; Aged; Alcoholism; Alkaline Phosphatase; Biopsy; Chemical and Drug Induced Liver Injury; Cholestasis; Chronic Disease; Enzymes; Fatty Liver; Female; Hepatitis A; Histocytochemistry; Humans; Hydroxybutyrate Dehydrogenase; Liver; Liver Cirrhosis; Liver Diseases; Male; Middle Aged

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Choline; Galactosamine; Hepatitis A; Histocytochemistry; Humans; Liver Diseases; Orotic Acid; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Electron Transport Complex IV; Enzymes; Glucose-6-Phosphatase; Histocytochemistry; Leucyl Aminopeptidase; Liver; Malate Dehydrogenase; Male; Mitochondria, Liver; Oxidoreductases; Rats

Systemic infection of mice with Mycobacterium BCG leads to focal liver damage by producing many granulomas. By undefined mechanisms, this infection markedly enhances the animal's susceptibility to the lethal effect of endotoxin. Small doses of endotoxin given to BCG-infected mice were found to cause acute hepatic damage, as demonstrated by elevated activities of liver enzymes in serum and by morphologic alterations documented by light and electron microscopy and by histochemical technics. The morphologic alterations caused by endotoxin included glycogen depletion, mitochondrial swelling, disruption of the continuity of sinusoidal endothelium and focal injury characterized by marked vacuolization of hepatocytes and distension and fragmentation of rough endoplasmic reticulum. Histochemical studies revealed the apparent release of acid phosphatase from granules in the central portions of granulomas, and the release of beta-glucuronidase from the cytoplasm of hepatocytes.

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Endotoxins; Female; Glucuronidase; Glycolysis; Histological Techniques; Liver; Mice; Mice, Inbred Strains; Microscopy, Electron; Mycobacterium bovis; Mycobacterium Infections

Topics: Acid Phosphatase; Animals; Carcinogens; Chemical and Drug Induced Liver Injury; Dimethylamines; Female; Glucuronidase; Histocytochemistry; Injections, Intraperitoneal; Liver; Liver Glycogen; Lysosomes; Microscopy, Electron; Necrosis; Nitrosamines; Rats; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Bile Pigments; Biopsy; Central Nervous System; Chemical and Drug Induced Liver Injury; Copper; Esterases; Fatty Liver; Female; Glutamate Dehydrogenase; Hemolysis; Histocytochemistry; Liver; Liver Diseases; Necrosis; Organ Size; Sheep; Sheep Diseases; Succinate Dehydrogenase; Sulfates

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Bile Ducts; Biliary Tract Diseases; Bone and Bones; Carcinoma, Hepatocellular; Chemical and Drug Induced Liver Injury; Chromatography, Gel; Chromatography, Ion Exchange; Electrophoresis; Intestines; Isoenzymes; Kidney; Ligation; Liver; Liver Diseases; Liver Neoplasms; Male; Neoplasms, Experimental; Rats

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride; Cell Membrane; Chemical and Drug Induced Liver Injury; Glutamate Dehydrogenase; Liver; Lysosomes; Male; Methods; Microscopy, Electron; Mitochondria, Liver; Oxidoreductases; Rats; Rats, Inbred Strains; Sorbitol; Succinate Dehydrogenase; Surface-Active Agents; Time Factors

Topics: Acid Phosphatase; Animals; Carbohydrate Metabolism; Cathepsins; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Galactosidases; Lipid Metabolism; Liver; Lysosomes; Mushroom Poisoning; Peptides; Proteins; Rats; Sulfuric Acids

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Antilymphocyte Serum; Azathioprine; Bilirubin; Biopsy; Chemical and Drug Induced Liver Injury; Cholestasis; Dogs; Esterases; Female; Histocytochemistry; Liver; Male; Staining and Labeling; Succinate Dehydrogenase; Transaminases

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cordotomy; Histocytochemistry; Liver; Male; Microscopy, Electron; Rats; Rats, Inbred Strains

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Alkaloids; Animals; Chemical and Drug Induced Liver Injury; Electron Transport Complex IV; Esterases; Glucose-6-Phosphatase; Glutamate Dehydrogenase; Heterocyclic Compounds; Histocytochemistry; Kidney Diseases; Kidney Tubules; Liver; Liver Diseases; Male; Necrosis; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Chloroquine; Cytoplasmic Granules; Glucuronidase; Histocytochemistry; Liver; Lysosomes; Male; Microscopy, Electron; Necrosis; Rats

Topics: Acid Phosphatase; Animals; Carbon Disulfide; Chemical and Drug Induced Liver Injury; Fats; Female; Histocytochemistry; Injections, Intraperitoneal; Liver; Liver Function Tests; Liver Glycogen; Male; Microscopy, Electron; Rats; Staining and Labeling

Topics: Acid Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Chloroform; Endoplasmic Reticulum; Ethers; Halothane; Histocytochemistry; Liver; Rats; RNA; Trichloroethylene

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Liver; Lysosomes; Microscopy, Electron; Rats; Surface-Active Agents

Topics: Acid Phosphatase; Animals; Antioxidants; Body Weight; Chemical and Drug Induced Liver Injury; Depression, Chemical; Diet; DNA; Female; Hypertrophy; Liver; Male; Organ Size; Phenols; Rats; Reproduction; RNA; Sex Factors; Time Factors

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Glucose-6-Phosphatase; Glucuronidase; Glutamate Dehydrogenase; L-Lactate Dehydrogenase; Liver; Male; Microsomes; Rats

Topics: Acid Phosphatase; Alkaloids; Animals; Chemical and Drug Induced Liver Injury; Esterases; Histocytochemistry; Liver Diseases; Lysosomes; Male; Rats

Topics: Acid Phosphatase; Animals; Berylliosis; Blood Glucose; Calcium; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; DNA; Glucose; Isocitrate Dehydrogenase; Leucine; Lipids; Liver; Liver Glycogen; Lysosomes; Male; Microsomes; Mitochondria; Nitrosamines; Organ Size; Oxygen Consumption; Phosphoglucomutase; Proteins; Rats

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Aspartic Acid; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Dihydrolipoamide Dehydrogenase; Guinea Pigs; Liver; Oxidoreductases; Rats

Topics: Acid Phosphatase; Adenosine Triphosphatases; Amino Acids; Animals; Asparagine; Aspartic Acid; Bilirubin; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Esterases; Glucose-6-Phosphatase; Hepatitis; Histocytochemistry; Humans; Lipid Metabolism; Liver; Liver Function Tests; Nucleic Acids; Oxidoreductases; Rats; Sulfobromophthalein

Topics: Acid Phosphatase; Animals; Cell Nucleus; Chemical and Drug Induced Liver Injury; Cytoplasm; Esterases; Female; Glycosides; Liver; Lysosomes; Male; Mice; Promethazine; Rats

Topics: Acid Phosphatase; Adenosine Triphosphatases; Aflatoxins; Alkaline Phosphatase; Animals; Aspergillus; Carcinogens; Chemical and Drug Induced Liver Injury; Endoplasmic Reticulum; Liver; Microscopy, Electron; Mitochondria; Poultry; Toxins, Biological

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride; Cathepsins; Chemical and Drug Induced Liver Injury; Dimethyl Sulfoxide; Ethionine; Glucose-6-Phosphatase; Glucuronidase; Liver; Oxidoreductases; Rats; Succinate Dehydrogenase; Sulfatases

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Chemical and Drug Induced Liver Injury; Cholinesterases; Clinical Enzyme Tests; In Vitro Techniques; Liver; Phosphorus; Rats

1. An investigation has been made of the changes occurring in lysosomal enzyme activities during the early development of experimentally produced liver injury in the rat. Three enzymes have been studied: acid phosphatase, acid ribonuclease and beta-glucuronidase. Four different methods of inducing liver injury have been used: administration of carbon tetrachloride, thioacetamide, dimethylnitrosamine and the fungal toxin sporidesmin. 2. The majority of the data presented concern alterations produced by carbon tetrachloride. Despite the extensive central necrosis and accompanying fat accumulation which this poison produced in the liver, only small changes in the activity and latency of lysosomal enzymes could be detected. In the early (pre-necrotic) period of injury these changes were insignificant. At a late stage of injury, when extensive centrilobular necrosis was present, there were indications of lysosomal rupture. 3. The results obtained with the other three hepatotoxins were similar to those described for carbon tetrachloride in that no evidence of early lysosomal rupture was obtained during the pre-necrotic period. It is concluded that lysosomes probably play no role in the early development of the four types of liver injury studied but, instead, are involved in later scavenging processes.

Topics: Acid Phosphatase; Amides; Animals; Blood; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Glucuronidase; Hepatitis; Liver; Lysosomes; Nitrosamines; Promethazine; Rats; Ribonucleases; Sulfhydryl Compounds

Topics: Acid Phosphatase; Alkaline Phosphatase; Anabolic Agents; Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Liver Cirrhosis; Rabbits

Topics: Acid Phosphatase; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cytoplasm; Electrons; Fatty Liver; Hepatitis; Histocytochemistry; Humans; Liver; Lysosomes; Microscopy; Microscopy, Electron; Rats; Research

Topics: Acid Phosphatase; Chemical and Drug Induced Liver Injury; Copper; Electrons; Hepatitis; Histocytochemistry; Liver; Microscopy; Microscopy, Electron; Pigments, Biological; Rats; Research; Toxicology

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Cathepsins; Chemical and Drug Induced Liver Injury; Fatty Liver; Glucuronidase; In Vitro Techniques; Liver; Lysosomes; Rats; Ribonucleases; Subcellular Fractions; Sulfatases; Urate Oxidase

Topics: Acid Phosphatase; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Ethionine; Fluorenes; Hemosiderin; Hepatitis; Injections; Injections, Subcutaneous; Iron; Iron-Dextran Complex; Liver; Proteins; Rats; Research; Toxicology

Topics: 2-Acetylaminofluorene; Acid Phosphatase; Chemical and Drug Induced Liver Injury; Dextrans; Electrons; Fluorenes; Hemosiderin; Hepatitis; Iron; Iron-Dextran Complex; Liver; Microscopy; Microscopy, Electron; Rats; Research; Toxicology

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Amides; Bile; Bile Ducts; Bile Ducts, Intrahepatic; Capillaries; Chemical and Drug Induced Liver Injury; Hepatitis; Histocytochemistry; Jaundice; Jaundice, Obstructive; Pathology; Research; Sulfhydryl Compounds; Thiocyanates; Toxicology

Topics: Acid Phosphatase; Alkaline Phosphatase; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hepatitis; Kidney; Liver; Mice; Pharmacology; Research; Toxicology; Uranium; Uranyl Nitrate

Topics: Acid Phosphatase; Alkaline Phosphatase; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Electron Transport Complex II; Glycogen; Hepatitis A; Histocytochemistry; Metabolism; Pathology; Rabbits; Research; Skin; Succinate Dehydrogenase; Toxicology

Topics: Acid Phosphatase; Alkaline Phosphatase; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Hepatitis; Kidney; Liver; Liver Cirrhosis; Phosphoric Monoester Hydrolases; Polysaccharides; Rats; Research; Toxicology