glycogen and Carbon-Tetrachloride-Poisoning

This study investigates the protective effect of betanin against liver injury induced by carbon tetrachloride (CCl4) in common carp (Cyprinus carpio L.). The fish were treated with 1, 2, and 4 % betanin in fodder throughout the experiment. After 20 days of treatment, the fish were intraperitoneally injected with 20 % (v/v in peanut oil) CCl4 at a volume of 0.5 mL/kg body weight. The fish were killed 3 days after CCl4 intoxication, and then, histological and biochemical assays were performed. Results showed that CCl4-induced liver CYP2E1 activity, oxidative stress, and injury, as indicated by the depleted glycogen storage, increased serum aspartate aminotransferase (AST)/alanine aminotransferase (ALT) activities and liver histological damage. Compared with the CCl4 control group, the betanin-treated groups exhibited reduced CYP2E1 activity, decreased malondialdehyde level, increased liver antioxidative capacity (increased glutathione level and superoxide dismutase and catalase activities), increased liver glycogen storage, and reduced serum AST/ALT activities, with significant differences in the 2 and 4 % groups (p < 0.05). Histological assay further confirmed the protective effect of betanin. In conclusion, betanin attenuates CCl4-induced liver damage in common carp. Moreover, the inhibition of CYP2E1 activity and oxidative stress may have significant roles in the protective effect of betanin.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Betacyanins; Carbon Tetrachloride Poisoning; Carps; Chemical and Drug Induced Liver Injury; Cytochrome P-450 CYP2E1; Glycogen; Liver; Oxidative Stress; Random Allocation

The content of glycogen and lipids in the liver, relative liver weight, the volume of hepatocytes and their nuclei, nucleocytoplasmic index, content binucleated hepatocytes, the chemical composition of the bones of the injured limb segment was studied after 3, 7, 28 days after the fracture of the leg bone after fracture leg bone with background carbon tetrachloride intoxication in mice CBA (n = 134). After the fracture revealed functional changes in the liver at all stages of the experiment. The decrease in the liver glycogen content and lipids in the bone of the injured limb segment--collagen and phosphate--was found after fracture leg bone of against the background liver failure. Found that during the recovery period after leg bone fracture liver condition affects mineral and organic composition of the bone injured limb segment.

Topics: Animals; Carbon Tetrachloride Poisoning; Collagen; Fractures, Bone; Glycogen; Hindlimb; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred CBA; Phosphates

Terminalia belerica Roxb. is one of the oldest medicinal herb of India, is an ingredient of Indian Ayurvedic drug 'triphala' used for the treatment of digestion and liver disorders. Present study is aimed to evaluate the protective effect of Terminalia belerica fruit extract and its active principle, gallic acid (3,4,5-trihydroxybenzoic acid) at different doses against carbon tetrachloride intoxication. Toxicant caused significant increase in the activities of serum transaminases and serum alkaline phosphatase. Hepatic lipid peroxidation level increased significantly whereas significant depletion was observed in reduced glutathione level after carbon tetrachloride administration. A minimum elevation was found in protein content on the contrary a significant fall was observed in glycogen content of liver and kidney after toxicant exposure. Activities of adenosine triphosphatase and succinic dehydrogenase inhibited significantly in both the organs after toxicity. Treatment with TB extract (200, 400 and 800mg/kg, p.o.) and gallic acid (50, 100 and 200mg/kg, p.o.) showed dose-dependent recovery in all these biochemical parameters but the effect was more pronounced with gallic acid. Thus it may be concluded that 200mg/kg dose of gallic acid was found to be most effective against carbon tetrachloride induced liver and kidney damage.

Topics: Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Dose-Response Relationship, Drug; Enzymes; Female; Gallic Acid; Glutathione; Glycogen; Herb-Drug Interactions; Kidney; Lipid Peroxidation; Liver; Medicine, Ayurvedic; Plant Extracts; Protective Agents; Proteins; Rats; Rats, Sprague-Dawley; Silymarin; Terminalia

Using cytofluorimetric and biochemical studies on serial supravital liver punctate biopsies, effects of chorionic gonadotropin (CG) on recovery of hepatocyte glycogen-forming function in the cirrhotically altered rat liver were analyzed. The biopsies were taken first from rats with experimental cirrhosis produced by their 6-month-long poisoning with the hepatotoxic poison CCl4, then from the same animals in 1, 3, and 6 month after cessation of their poisoning, either on treatment with CG or with no treatment. In smears of isolated hepatocytes, the contents of the total glycogen (TG) and of its labile and stable fractions (LF and SF, respectively) were measured. In liver homogenates, activities of glucose-6-phosphatase (G6Pase), glycogen phosphorylase, and glycogen synthetase were determined. It was found that the threefold increased TG content in hepatocytes of cirrhotic liver returned to the normal level in 3 months without treatment, while as soon as in 1 month in the case of the treatment with CG. The CG treatment for 3 months resulted in normalization of the glycogen fraction composition that had been changed in cirrhotic liver, whereas without treatment, the glycogen LF/SF ratio remained changed even after 6 months after cessation of the poisoning with CCl4. Activity of G6Pase was fourfold reduced in cirrhosis; in 3 months after the end of poisoning, under effect of CG, the activity increased to the normal level, but somewhat decreased subsequently. In the animals that were not treated with CG, the decrease in the G6Pase activity after the cessation of the CCl4 poisoning was even more marked than in the CG-treated rats. Activities of two other enzymes of glycogen metabolism did not differ statistically significantly from the norm throughout the entire experiment. The data obtained indicate that the use of CG for rehabilitation of the glycogen-forming function of the cirrhotically altered liver is more efficient than other ways of treatment studied previously, such as partial hepatectomy or a high-carbohydrate diet.

Topics: Animals; Carbon Tetrachloride Poisoning; Chorionic Gonadotropin; Fluorescence; Glucose-6-Phosphatase; Glycogen; Glycogen Synthase; Hepatocytes; Liver; Liver Cirrhosis, Experimental; Male; Periodic Acid-Schiff Reaction; Phosphorylases; Rats; Staining and Labeling

Topics: Animals; Bilirubin; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury, Chronic; Glycogen; Liver; Male; Malondialdehyde; Rats; Soybean Proteins

By cytofluorometric and biochemical methods the content of total glycogen and its fractions was investigated on the smears of isolated liver cells: labile fraction (LF) and stable fraction (SF) and also activities of glycogen phosphorylase (GP), glucose-6-phosphatase (G-6-Pase) and glycogen synthase. The material was obtained from serial liver biopsies from each investigated animal prior to CCl4 action (control), with cirrhosis (6 months of CCl4 poisoning) and 1, 3 and 6 months after CCl4 poisoning was finished. It was shown that chronic CCl4 poisoning induced a typical liver cirrhosis accompanied with the 2-3 times increase in the total glycogen content, in comparison with the norm, with the decrease in LF to 53%, and also with the fall of G-6-Pase and GP activities by 82 and 25%, resp. After 1, 3 and 6 months following poisoning cessation, the lobule structure, infringed due to cirrhosis, was not restored. But functional parameters of the cirrhotic liver were seen gradually recovering without CCl4 poisoning. The application of carbohydrate rich diet favoured a most complete rehabilitation: the content of total glycogen and its fractions and the activity of G-6-Pase and GP returned to the normal level.

Topics: Animals; Carbon Tetrachloride Poisoning; Dietary Carbohydrates; Flow Cytometry; Glycogen; Liver; Liver Cirrhosis, Experimental; Male; Rats

To determine the effect of insulin-like growth factor I (IGF-I) on glucose metabolism in cirrhosis, a 2-h euglycemic clamp with IGF-I (0.65 nmol.kg-1.min-1) or insulin (12 pmol.kg-1.min-1) was performed in awake rats with carbon tetrachloride-induced liver cirrhosis. Rates of [3-3H]glucose-determined whole body glucose turnover were similar in the fasting state in cirrhotic and control rats (36.4 +/- 2.6 and 37.7 +/- 2.8 mumol.kg-1.min-1, respectively). In the control group, IGF-I and insulin had similar effects on turnover (81.6 +/- 27.0 and 76.1 +/- 9.9 mumol.kg-1.min-1), muscle glycogen synthesis (47.5 +/- 12.3 and 37.5 +/- 2.5 nmol.g muscle-1.min-1), and suppression of endogenous glucose production (EGP; -54 +/- 14 and -60 +/- 12%). Cirrhotic rats were markedly insulin resistant, reflected by a 43% reduction of turnover (43.8 +/- 9.4 mumol.g muscle-1.min-1; P = 0.03), a 73% reduction in muscle glycogen synthesis (10.2 +/- 3.4 nmol.g muscle-1.min-1; P < 0.0001), and a diminished suppression of EGP (-32 +/- 17% vs. control: -56 +/- 14%; P < 0.05). In contrast, during the IGF-I clamps, turnover increased threefold in the cirrhotic rats (P = 0.001), rates of muscle glycogen synthesis were 7.4 times higher than during the insulin stimulation (P < 0.0001), and EGP was suppressed by 80 +/- 12% (P < 0.05). In conclusion, insulin resistance in cirrhotic rats is mostly due to defects in insulin-stimulated muscle glycogen synthesis, and the ability of IGF-I to stimulate muscle glycogen synthesis as well as suppress EGP is maintained in cirrhotic rats. These findings suggest that alterations in both hepatic and peripheral glucose metabolism in patients with cirrhosis might be amenable to IGF-I therapy.

Topics: Animals; Blood Glucose; Carbon Tetrachloride Poisoning; Glucose; Glucose Clamp Technique; Glycogen; Infusions, Intravenous; Insulin; Insulin-Like Growth Factor I; Liver; Liver Cirrhosis, Experimental; Male; Muscle, Skeletal; Rats; Rats, Sprague-Dawley

The influence of several Chinese drugs on the glycogen synthesizing function of normal and carbon tetrachloride-injured hepatocytes was investigated. Hepatocytes prepared from rats fasted for 16 h were incubated with 50 mmol/L glucose. Glycogen content was determined 30 and 90 min after incubation with normal and CCl4-injured cells, respectively. Insulin was used as positive control which increased glycogen content and the data coincided with that in the literature. The following results were obtained (1) Biphenyl-dimethyl-dicarboxylate (BDD) in 100 micrograms/ml concentration increased glycogen content of normal hepatocytes by 88%. It protected cells against CCl4-injury:BDD 10 micrograms/ml remarkably decreased CCl4-induced reduction of glycogen and 100 micrograms/ml showed complete protection. (2) Tremella poly-saccharide slightly increased glycogen content in normal cells, but in a concentration of 100 micrograms/ml it decreased CCl4-induced reduction of glycogen significantly. (3) Low concentration of norcatharidin (10 micrograms/ml) increased glycogen content of normal cells, but at 100 micrograms/ml concentration this effect disappeared. Furthermore, it intensified the toxic effect of CCl4 on glycogen at 10-100 micrograms/ml. (4) CL1500 (100 micrograms/ml) increased glycogen content of normal cells, but it intensified CCl4-injury effect on glycogen at the same concentration.

Topics: Animals; Basidiomycota; Carbon Tetrachloride Poisoning; Cells, Cultured; Dioxoles; Drugs, Chinese Herbal; Female; Glycogen; Liver; Malonates; Polysaccharides; Rats; Rats, Inbred Strains

Topics: Animals; Carbon Tetrachloride Poisoning; Glycogen; Liver Glycogen; Male; Muscles; Rats; Stimulation, Chemical; Vitamin B 12

Topics: Animals; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cytoplasm; Endoplasmic Reticulum; Glycogen; Golgi Apparatus; Lipids; Liver; Liver Regeneration; Lysosomes; Male; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Mitochondria

Topics: Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cold Temperature; Drug Tolerance; Glutamate Dehydrogenase; Glycogen; Histocytochemistry; Lipid Metabolism; Liver; Liver Diseases; Mice; Necrosis; Staining and Labeling; Time Factors

Topics: Aging; Alanine Transaminase; Amino Acids; Animals; Aspartate Aminotransferases; Blood Glucose; Carbon Tetrachloride Poisoning; Catalase; Chemical and Drug Induced Liver Injury; Glycogen; Mice; Rabbits; Rats; Trace Elements; Vitamins; Water-Electrolyte Balance

Topics: Animals; Bile; Bile Acids and Salts; Carbon Tetrachloride Poisoning; Cholesterol; Glycogen; In Vitro Techniques; Liver; Male; Perfusion; Rats; Stimulation, Chemical; Taurine; Triglycerides

Topics: Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Choline; Choline Deficiency; Dietary Fats; Dietary Proteins; Fatty Liver; Female; Glycogen; Histocytochemistry; Injections, Subcutaneous; Mice

Topics: Animals; Biotransformation; Carbon Tetrachloride Poisoning; Cell Membrane; Cell Nucleus; Cytoplasm; Endoplasmic Reticulum; Glycogen; Golgi Apparatus; In Vitro Techniques; Liver Cirrhosis, Experimental; Liver Regeneration; Microscopy; Microscopy, Electron; Rats

Topics: Animals; Carbon Tetrachloride Poisoning; Denervation; Dogs; Glycogen; Hepatic Artery; Lipids; Liver; Manometry; Oxygen Consumption

Topics: Animals; Capillaries; Carbon Tetrachloride Poisoning; Cell Nucleus; Cytoplasm; DNA; Glycogen; Guinea Pigs; Liver Regeneration; Mice; Vertebrates

Topics: Alkaline Phosphatase; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Female; Glycogen; Histocytochemistry; Humans; Oxidoreductases; Pathology; Pharmacology; Rats; Research; Toxicology; Uterus

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: Alkaline Phosphatase; Animals; Bile; Carbohydrate Metabolism; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Dogs; Glycogen; Hepatitis; Hormones; Lipid Metabolism; Liver; Pharmacology; Pineal Gland; Rats

Topics: Animals; Blood Glucose; Carbohydrate Metabolism; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Glucose; Glycogen; Glycogenolysis; Liver; Liver Glycogen; Mice

Topics: Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Glycogen; Liver; Liver Glycogen