tannins and Liver-Diseases

Pistacia integerrima with a common name crab's claw is an ethnobotanically important tree native to Asia. Traditionally plant parts particularly its galls have been utilized for treatment of cough, asthma, dysentery, liver disorders and for snake bite. Plant mainly contains alkaloids, flavonoids, tannins, saponins and sterols in different parts including leaf, stem, bark, galls and fruit. A number of terpenoids, sterols and phenolic compounds have been isolated from Pistacia integerrima extracts. Plant has many biological activities including anti-microbial, antioxidant, analgesic, cytotoxicity and phytotoxicity due to its chemical constituents. This review covers its traditional ethnomedicinal uses along with progresses in biological and phytochemical evaluation of this medicinally important plant species and aims to serve as foundation for further exploration and utilization.

Topics: Alkaloids; Asthma; Cough; Dysentery; Ethnobotany; Flavonoids; Humans; Liver Diseases; Phytochemicals; Phytotherapy; Pistacia; Plant Extracts; Saponins; Snake Bites; Sterols; Tannins

Most clinical problems due to plant exposures result from experimentation with or overt abuse of plant parts and extracts. Plant exposures may present as complex pharmacologic problems that challenge the diagnostic and therapeutic skills of the physician. Although specific physiologic antagonists (antidotes) may exist for specific intoxications, basic decontamination and supportive techniques are often all that may be offered.

Topics: Adult; Alkaloids; Autonomic Nervous System Diseases; Cardiovascular Diseases; Central Nervous System Diseases; Child; Child, Preschool; Dermatitis, Contact; Emergencies; Gastroenteritis; Glycosides; Hematologic Diseases; Humans; Kidney Diseases; Liver Diseases; Magnoliopsida; Oils; Plant Extracts; Plant Poisoning; Plants, Toxic; Resins, Plant; Tannins

Exposures to plants generate an exceptional amount of public concern, especially plant ingestions by children. Most clinical problems, however, involve older age groups as a result of experimentation with or overt abuse of plant parts and extracts. Of mounting concern is the sometimes uninformed and massive use of herbal preparations, currently widely available and in popular vogue. Plant exposures, from whatever source, may present as complex pharmacologic problems that may challenge the diagnostic and therapeutic skills of the physician. Although specific physiologic antagonists (antidotes) may exist for specific intoxications, basic decontamination and supportive techniques are many times all that may be offered.

Topics: Adult; Alkaloids; Cardiovascular Diseases; Child; Cyanides; Dermatitis, Contact; Emergencies; Female; Gastroenteritis; Glycosides; Hematologic Diseases; Humans; Kidney Diseases; Liver Diseases; Magnoliopsida; Male; Mouth Mucosa; Nervous System Diseases; Oils, Volatile; Plant Poisoning; Plants, Edible; Plants, Medicinal; Plants, Toxic; Resins, Plant; Tannins

Topics: Animals; Arsenicals; Chemical and Drug Induced Liver Injury; Chloroform; Chlorpromazine; Contraceptives, Oral; Drug Hypersensitivity; Humans; Isoniazid; Liver Diseases; Steroids; Tannins; Tetracycline

Azidothymidine (AZT) is known to decrease HIV virus replication and is one of the most frequently prescribed antiretroviral drugs used for AIDS treatment. Dose-limiting toxicities are the major curse associated with AZT therapy. Recently, we have reported that tannic acid; a PARG inhibitor prevents cisplatin induced nephrotoxicity. The present work was conceived to study the effect of tannic acid on AZT induced hepatotoxicity and genotoxicity. AZT induces increase in plasma levels of ALT, AST and alkaline phosphatase along with increase in micronucleus (MN) count in peripheral blood. Suggesting, AZT is hepatotoxic and genotoxic to mice. Treatment of tannic acid protects AZT induced hepatotoxicity by decreasing the ALT, AST and alkaline phosphatase levels. It also significantly reduces the oxidative damage by preventing reduction in glutathione and decreasing the level of malondialdehyde in liver of AZT treated mice. In addition, tannic acid decreases the PARG expression, PARP cleavage and histone H3 acetylation in liver of AZT treated mice. Moreover, treatment of tannic acid also decreases MN count in peripheral blood, suggesting its anti-mutagenic effect. In light of these findings we suggest the potential role of tannic acid treatment in preventing AZT induced toxicity.

Topics: Acetylation; Alanine Transaminase; Alkaline Phosphatase; Animals; Anti-HIV Agents; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; DNA Damage; Glycoside Hydrolases; Histones; Liver; Liver Diseases; Malondialdehyde; Mice; Micronucleus Tests; Oxidative Stress; Poly (ADP-Ribose) Polymerase-1; Poly(ADP-ribose) Polymerases; Tannins; Zidovudine

The polyphenol-rich fraction (WP, 45% polyphenol) prepared from the kernel pellicles of walnuts was assessed for its hepatoprotective effect in mice. A single oral administration of WP (200 mg/kg) significantly suppressed serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) elevation in liver injury induced by carbon tetrachloride (CCl 4), while it did not suppress d-galactosamine (GalN)-induced liver injury. In order to identify the active principles in WP, we examined individual constituents for the protective effect on cell damage induced by CCl 4 and d-GalN in primary cultured rat hepatocytes. WP was effective against both CCl 4- and d-GalN-induced hepatocyte damages. Among the constituents, only ellagitannins with a galloylated glucopyranose core, such as tellimagrandins I, II, and rugosin C, suppressed CCl 4-induced hepatocyte damage significantly. Most of the ellagitannins including tellimagrandin I and 2,3- O-hexahydroxydiphenoylglucose exhibited remarkable inhibitory effect against d-GalN-induced damage. Telliamgrandin I especially completely suppressed both CCl 4- and d-GalN-induced cell damage, and thus is likely the principal constituent for the hepatoprotective effect of WP.

Topics: Animals; Carbon Tetrachloride; Cells, Cultured; Chemical and Drug Induced Liver Injury; Flavonoids; Galactosamine; Gallic Acid; Glucosides; Hydrolysis; Juglans; Liver Diseases; Phenols; Polyphenols; Rats; Seeds; Tannins

Punicalagin and punicalin were isolated from the leaves of Terminalia catappa L., a Combretaceous plant distributed throughout tropical and subtropical beaches, which is used for the treatment of dermatitis and hepatitis. Our previous studies showed that both of these compounds exert antioxidative activity. In this study, the antihepatotoxic activity of punicalagin and punicalin on acetaminophen-induced toxicity in the rat liver was evaluated. After evaluating the changes of several biochemical functions in serum, the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were increased by acetaminophen administration and reduced by punicalagin and punicalin. Histological changes around the hepatic central vein and oxidative damage induced by acetaminophen were also recovered by both compounds. The data show that both punicalagin and punicalin exert antihepatotoxic activity, but treatment with larger doses enhanced liver damage. These results suggest that even if punicalagin and punicalin have antioxidant activity at small doses, treatment with larger doses will possibly induce some cell toxicities.

Topics: Acetaminophen; Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Hydrolyzable Tannins; Lipid Peroxidation; Liver; Liver Diseases; Male; Plant Extracts; Plants, Medicinal; Rats; Rats, Wistar; Rosales; Tannins

Oak poisoning occurred in crossbred cattle due to eating immature tender oak (Quercus incana) leaves. Mortality was 70%. The animals exhibited anorexia, severe constipation and brisket edema. The feces were hard, pelleted and coated with blood and mucous. Significant reductions in blood hemoglobin and mean corpuscular hemoglobin, and significant elevations in serum bilirubin were observed. Serum urea nitrogen and creatinine were greatly increased. There was bilirubinuria, proteinuria, hypoproteinemia and hypocalcemia, and greatly increased activities of serum aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. The levels of tannins and condensed tannins were 97.7 mg tannic acid equivalent and 5.8 mg catechin equivalent/g of dry leaves. There was extensive nephro- and hepatotoxicity in the affected cattle due to hydrolysable tannins and simple phenols in the oak leaves.

Topics: Anemia, Hemolytic; Animals; Anorexia; Blood Cells; Blood Chemical Analysis; Cattle; Cattle Diseases; Constipation; Edema; Feces; Hypothermia; Kidney Diseases; Liver Diseases; Phenols; Plant Poisoning; Polyuria; Tannins; Trees

A study was conducted to identify and characterise the toxic principle in Terminalia oblongata, commonly known as yellow-wood. Crude aqueous extracts of yellow-wood leaf were found to produce the same liver lesion in mice as has been reported in ruminants. The hepatotoxic fraction was isolated and identified as a hydrolysable vegetable tannin called punicalagin. When given orally, the dose required to produce toxicity was at least 20 times greater than when given intraperitoneally. Following a given dose of punicalagin, the onset and severity of liver necrosis was found to be related to the time interval after dosing. In addition to punicalagin, an unidentified nephrotoxic substance was found which was capable of producing avascular renal necrosis without liver necrosis.

Topics: Administration, Oral; Animals; Chemical and Drug Induced Liver Injury; Injections, Intraperitoneal; Kidney Diseases; Liver Diseases; Male; Mice; Microscopy, Electron; Necrosis; Plants, Toxic; Tannins

Topics: Animals; Antioxidants; Depression, Chemical; Drugs, Chinese Herbal; Free Radicals; Lipid Peroxidation; Lipid Peroxides; Liver Diseases; Microsomes, Liver; Mitochondria, Liver; Tannins

Topics: Antibodies; Antigens; Aorta; Aortic Diseases; Collagen Diseases; Complement Fixation Tests; Creatine Kinase; Endocrine System Diseases; Esophageal Diseases; Fluorescent Antibody Technique; Heart Diseases; Hemagglutination Tests; Hematologic Diseases; Humans; Immunoglobulins; Inflammation; Kidney Diseases; Liver Diseases; Lung Diseases; Microbial Collagenase; Nervous System Diseases; Precipitin Tests; Streptococcus; Tannins; Vascular Diseases

Topics: Acetamides; Animals; Antigens; Beryllium; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Common Bile Duct; Female; Fluorescent Antibody Technique; Goats; Immune Sera; Immunodiffusion; Liver Diseases; Male; Organ Specificity; Proteinuria; Rabbits; Rats; Tannins; Urethane

Topics: Acute Disease; Adolescent; Adult; Aged; Anticonvulsants; Antitubercular Agents; Azathioprine; Blood Transfusion; Chemical and Drug Induced Liver Injury; Child; Female; Halothane; Hepatic Encephalopathy; Hepatitis A; Hepatitis B; Humans; Infant; Leukocytosis; Liver Diseases; Male; Middle Aged; Necrosis; Penicillins; Prothrombin Time; Sulfonamides; Tannins

Topics: Barium Sulfate; Body Weight; Contrast Media; Humans; Intestinal Mucosa; Liver Diseases; Necrosis; Tannins

Topics: Chemical and Drug Induced Liver Injury; Fatty Liver; Hepatitis; Liver Diseases; Liver Glycogen; Necrosis; Pathology; Rabbits; Research; Tannins; Toxicology

The LD(50) +/- S.E. of tannic acid given orally to albino rats was found to be 2.26+/-0.083 g. per kg. body weight, which is higher than its apparent LD(50) when given per rectum. The immediate cause of death was respiratory failure preceded by convulsions when death occurred early and by hypothermic cachexia when death was delayed. Death was associated with a progressively developing hepatic necrosis and nephritis and a temporary acute gastroenteritis. It was accompanied by loss of weight and edema in many organs, evidence of stimulation of the spleen, adrenal cortex and testes, and atrophy of the thymus. Recovery in survivors was associated with a temporary increase in weight of the spleen and testes and persistence of loss of weight in the adrenal, pyloric stomach, and skin.

Topics: Cachexia; Chemical and Drug Induced Liver Injury; Edema; Gastroenteritis; Hepatitis; Hepatitis A; Hypothermia; Liver Diseases; Nephritis; Pathology; Rats; Research; Seizures; Spleen; Tannins; Toxicology

Topics: Adolescent; Adult; Aged; Barium Sulfate; Child; Child, Preschool; Enema; Humans; Infant; Liver Diseases; Male; Necrosis; Tannins

Topics: Acetonitriles; Amides; Benzene; Bromobenzenes; Cyanides; Liver; Liver Diseases; Necrosis; Tannins; Thioacetamide

Tannic acid contained in the barium enema was found to have been the sole known potential hepatotoxin in four of the five cases of fulminating fatal liver failure that occurred in a 213-bed hospital over a period of 27 months. In the other case halothane anesthesia had also been administered. Autopsies (performed on four of the cases) did not suggest viral hepatitis but showed substantially indentical hepatic changes, not unlike those reported in the past following tannic acid exposure. Proof is not claimed that tannic acid was the cause of these deaths, but further investigation regarding the safety of its administration in barium enemas is advocated.

Topics: Barium; Barium Sulfate; Chemical and Drug Induced Liver Injury; Enema; Hepatitis; Hepatitis A; Humans; Liver Diseases; Radiography, Abdominal; Tannins; Toxicology