acid-phosphatase and Carbon-Tetrachloride-Poisoning

Aphanamixis polystachya is a traditional medicinal plant of the Meliaceae family in India. A crude ethanolic extract of the leaf of this plant shows a beneficial effect on toxic liver injury. Its antihepatotoxic activity was evaluated on carbon tetrachloride (CCl4)-induced liver injury in a rat model. The assessment of hepatoprotective activity was evaluated by measuring the activities of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), alkaline phosphatase (ALP), acid phosphatase (ACP) and lactate dehydrogenase (LDH), serum total bilirubin and albumin and histology of the liver. The crude leaf extract significantly inhibits the enhanced ASAT, ALAT, ALP, ACP and LDH activities released from the CCl4-intoxicated animals. It also ameliorated the depressed value of serum albumin and the enhanced value of total bilirubin in plasma caused by CCl4 intoxication. The study showed that the crude ethanolic extract from A. polystachya leaves provided protection against acute carbon tetrachloride-induced liver damage.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Bilirubin; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Disease Models, Animal; L-Lactate Dehydrogenase; Liver; Male; Plant Extracts; Plants, Medicinal; Rats; Serum Albumin

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

Changes in the total activity of acid phosphatase in the liver as well as changes in the enzyme activity in hepatocytes and connective tissue cells of fibrosis layers were investigated, using quantitative histochemical method, in the process of mouse cirrhosis involution. After discontinuation of CCl4 injection, the animals with cirrhosis were divided into two groups. In the first group the resection of the left lobe of the liver was performed. The animals of the second group were not subject to operation. The results demonstrate that there is a close correlation between lysosomal hydrolase activity of hepatocytes and connective tissue cells of the liver and collagen resorption during cirrhosis involution. The most intensive lysis of collagen takes place within the first three weeks of cirrhosis involution in both experimental groups. Partial resection in cirrhosis has no significant effect on the changes and level of total activity of lysosomal hydrolase enzymes in the liver during cirrhosis involution.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Liver; Liver Cirrhosis, Experimental; Male; Mice

The distribution of acid phosphatase in liver cirrhosis, as well as in its reverse development, was investigated in mice using histochemistry and electron histochemistry methods. Histochemistry demonstrated a sharp activity increase of acid phosphatase (as compared with the same in the material of partial hepatectomy) in liver cells (especially hepatocytes) during liver cirrhosis regression 10 days after a partial hepatectomy. Electron histochemistry has shown the enzyme withdraw out of hepatocytes and connective tissue cells of fibrotic stratum in the extra-cell medium. The reaction product localized on the neighbouring collagen fibres giving evidence that during reverse development of liver cirrhosis the lisosomal enzyme release from specified cells by means of exocytosis and they are involved in the lysis of collagen.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Hepatectomy; Histocytochemistry; Liver; Liver Cirrhosis; Liver Regeneration; Lysosomes; Male; Mice; Microscopy, Electron; Time Factors

The object of the study was rats myocardium. Tissue samples were examined 3, 6 and 12 hours after carbon tetrachloride treatment. The poison was administered by a gastric tube in single dose of 0.6 ml/100 g body weight. The examination carried out by the histochemical method revealed changes in the intensity of enzymatic reaction, whereas due to the Selye staining fuosynophylic fibres were found.

Topics: Acid Phosphatase; Acute Disease; Animals; Carbon Tetrachloride Poisoning; Glycerolphosphate Dehydrogenase; Heart; Histocytochemistry; Male; Myocardium; Rats; Rats, Inbred Strains; Succinate Dehydrogenase

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

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Hepatitis, Alcoholic; Humans; Lipid Peroxides; Liver Diseases; Lysosomes; Male; Rats

Liver cirrhosis was induced in male Wistar rats weighing 200-250 g by subcutaneous injection of 0.25 ml of a 10% CCl4 solution per 100 g bw. Kupffer cells were stimulated with prodigiozan which was introduced at a 10-day interval in the course of fibrosis development. Under stimulation the injury to the parenchyma decreased; the total number of Kupffer macrophages and the degree of mononuclear infiltration of liver tissue increased, while fibroplasia diminished. The content of hydroxyproline in liver homogenates of prodigiozan-stimulated rats was half as much as compared with controls.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Kupffer Cells; Liver; Liver Cirrhosis, Experimental; Male; Polysaccharides, Bacterial; Prodigiozan; Rats; Rats, Inbred Strains; Thymidine

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

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

The author examined the enzymatic activity in the intestinal mucosa under the conditions of rat liver cirrhosis, experimentaly induced by carbon tetrachloride. There was a correlative connection between liver damage and the functional activity of the intestines, manifested by the inhibition of the activity of the membrane enzymes-alkaline phosphatase and aminopetidase as well as the activity of acid phosphatase and succinic dehydrogenase.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Aminopeptidases; Animals; Carbon Tetrachloride Poisoning; Clinical Enzyme Tests; Enzyme Activation; Enzyme Repression; Intestinal Mucosa; Intestine, Small; Liver Cirrhosis, Experimental; Rats; Succinate Dehydrogenase

In order to clarify the action of drugs for liver disease, the effect of protoporphyrin (PP) on CCl4-induced liver injury was studied. Attention was given to the levels of lysosomal enzymes, some components of the liver, and inhibition of enzymes and lysis of lysosomal membranes by lipid peroxides. Administration of PP to CCl4-poisoned rats was found to prevent the decrease in lysosomal lipolytic enzyme level in the liver, but not in other enzyme levels tested. The inhibition of lipolytic enzyme by CCl4 administered may be partially involved in lipid accumulation in the liver. A dose of PP administered to CCl4-poisoned rats for 8 days depressed the neutral lipid content in the liver nearly to the control value. Methyl linoleate hydroperoxide (hydroperoxide) at a lower concentration of 10(-6)% inhibited the lipolytic enzyme acitivity by 30% and in concentrations ranging from 10(-4) to 10(-3)% inhibited beta-glucuronidase activity. Addition of PP to the medium containing 10(-6) to 10(-5)% hydroperoxide and alpha-tocopherol reduced the enzyme inhibition further than in the absence of PP. The hydroperoxide in concentrations varying from 10(-6) to 10(-3)% caused a partial lysis of liver lysosomal membranes, but addition of PP slightly reduced the damage by the hydroperoxide in concentration lower than 10(-5)%.

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Glucuronidase; Linoleic Acids; Lipase; Lipid Metabolism; Liver; Lysosomes; Male; Membranes; Peroxides; Phosphoric Diester Hydrolases; Porphyrins; Protoporphyrins; Rats; Vitamin E

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

Changes in protein elution patterns and among others in the distribution profiles of some isozymes, as the lysosomal acid phosphatase, the microsomal alkaline phosphatase, the cytoplasmic fraction of aspartate aminotransferase and some fractions of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, have been found in liver experimental fatty change induced in rats by carbon tetrachloride and ethionine. The possible meaning of these changes is discussed.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Cytoplasm; Ethionine; Female; Fructose-Bisphosphate Aldolase; Glucosephosphate Dehydrogenase; Glucuronidase; Isoenzymes; Liver; Lysosomes; Microsomes, Liver; Phosphogluconate Dehydrogenase; Rats

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; 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; Animals; Capillaries; Carbon Tetrachloride Poisoning; Female; Glucuronates; Glucuronidase; Glycosaminoglycans; Glycosides; Hexosaminidases; Liver; Liver Cirrhosis; Liver Cirrhosis, Experimental; Microcirculation; Phenylhydrazines; Rats

Topics: Acid Phosphatase; Animals; Body Temperature; Carbon Isotopes; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Cystamine; Cysteamine; Cytochrome Reductases; Glucose-6-Phosphatase; In Vitro Techniques; Lipid Metabolism; Liver; Lysosomes; Male; Methyltransferases; Microsomes, Liver; Oxidation-Reduction; Rats; Ribonucleases; Time Factors

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; Animals; Carbon Tetrachloride Poisoning; Drug Antagonism; Ethylamines; Imipramine; In Vitro Techniques; Liver; Lysosomes; Malonates; Mitochondria, Liver; Mitochondrial Swelling; Permeability; Phenethylamines; Proadifen; Proteins; Rats; Ribonucleases; Statistics as Topic; Time Factors

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; 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; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Esterases; Female; Glucosephosphate Dehydrogenase; Glucosyltransferases; Lipids; Liver; Liver Glycogen; Malate Dehydrogenase; Oxidoreductases; Phosphorylase Kinase; Phosphorylases; Rats; RNA; Statistics as Topic; Succinate Dehydrogenase; Sulfhydryl Compounds

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

Topics: Acid Phosphatase; Acyltransferases; Alanine Transaminase; Alcohol Oxidoreductases; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Bile; Carbon Tetrachloride Poisoning; Cytoplasm; Glucose-6-Phosphatase; Glucosephosphate Dehydrogenase; Glutamate Dehydrogenase; Glutamates; Isocitrate Dehydrogenase; Isoenzymes; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; Liver; Lysosomes; Malate Dehydrogenase; Male; Mitochondria, Liver; Phosphoric Monoester Hydrolases; Rats; Ribosomes; Time Factors; Transferases

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Esterases; Histocytochemistry; Hydrolases; Lipase; Liver; Nucleotidases; Sciuridae

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; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Esterases; Kidney; Liver; Phosphoric Monoester Hydrolases; Rats

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

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Depression, Chemical; Fatty Liver; Lipid Metabolism; Liver; Liver Regeneration; Pyridoxine; Rats; Riboflavin; Thiamine

Topics: Acid Phosphatase; Aminocaproates; Animals; Antifibrinolytic Agents; Aprotinin; Carbon Tetrachloride Poisoning; Chymotrypsin; Cyclohexanecarboxylic Acids; Edema; Female; Fibrinolysin; Guinea Pigs; Inflammation; Kallikreins; Microbial Collagenase; Pancreatic Elastase; Peptides; Protease Inhibitors; Rats; Ribonucleases; Trypsin

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Creatinine; Diuresis; Endoplasmic Reticulum; Glucose-6-Phosphatase; Kidney; Kidney Tubules; Male; Microscopy, Electron; Mitochondria; Organ Size; Potassium; Rats; Sodium; Succinate Dehydrogenase; Water

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; Androgens; Animals; Carbon Tetrachloride Poisoning; Esterases; Estrogens; Histocytochemistry; Kidney Tubules; Male; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Anura; Carbon Tetrachloride Poisoning; Histocytochemistry; Kidney; Kidney Diseases; Kidney Tubules; Lipids; Male; Necrosis; Succinate Dehydrogenase

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; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Esterases; Histocytochemistry; Immunization, Passive; Rats; Spleen

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; Alcohol Oxidoreductases; Alkaline Phosphatase; Animals; Carbon Tetrachloride Poisoning; Carbonic Anhydrases; Dihydrolipoamide Dehydrogenase; Electron Transport Complex IV; Esterases; Histocytochemistry; L-Lactate Dehydrogenase; Liver; Liver Diseases; Male; Mice; Succinate Dehydrogenase; Zinc

Topics: Acid Phosphatase; Animals; Carbon Tetrachloride Poisoning; Golgi Apparatus; Lysosomes; Male; Phosphotransferases; Rats

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carbon Tetrachloride Poisoning; Esterases; Female; Fluorescence; Glucose-6-Phosphatase; Histocytochemistry; Liver; Male; Monoamine Oxidase; Rats; Staining and Labeling; Succinate Dehydrogenase

Accumulation of calcium in the mitochondria of rat liver parenchymal cells at 16 and 24 hours after poisoning with carbon tetrachloride is associated with an increase in amount of liver inorganic phosphate, the persistence of mitochondrial adenosine triphosphatase activity, and the formation of electron-opaque intramitochondrial masses in cells with increased calcium contents. These masses, which form within the mitochondrial matrix adjacent to internal mitochondrial membranes, resemble those observed in isolated mitochondria which accumulate calcium and inorganic phosphate; are present in a locus similar to that of electron opacities which result from electron-histochemical determination of mitochondrial ATPase activity; and differ in both appearance and position from matrix granules of normal mitochondria. After poisoning, normal matrix granules disappear from mitochondria prior to their accumulation of calcium. As calcium-associated electron-opaque intramitochondrial masses increase in size, mitochondria degenerate in appearance. At the same time, cytoplasmic membrane systems of mid-zonal and centrilobular cells are disrupted by degranulation of the rough endoplasmic reticulum and the formation of labyrinthine tubular aggregates. The increase in amount of inorganic phosphate in rat liver following poisoning is balanced by a decreased amount of phosphoprotein. These chemical events do not appear to be related, however, as the inorganic phosphate accumulated is derived from serum inorganic phosphate.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Adenosine Triphosphate; Alkaline Phosphatase; Animals; Calcium; Calcium Phosphates; Carbon Tetrachloride Poisoning; Cytoplasmic Granules; Glucose-6-Phosphatase; Liver; Microscopy, Electron; Mitochondria; 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; 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: 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