glycogen and Poisoning

Topics: Animals; Brain Chemistry; Diabetes Mellitus; Diuretics; Glycogen; Hepatolenticular Degeneration; Humans; Hypercholesterolemia; Hyperlipidemias; Liver; Liver Diseases; Poisoning; Skin Diseases; Thioctic Acid

The lethal and sublethal toxicity of Endosulfan on the African toad, Bufo regularis were evaluated to assess changes in behaviour and energy reserves. 96 hours LC50 was 0.730 mg/l while the estimated safe concentration was 0.07 mg/L indicating the high toxicity of the insecticide. Toads exposed to lethal concentrations of endosulfan showed dose-dependent behavioural abnormalities with more pronounced poisoning symptoms occurring at higher concentrations. The pesticide caused differential increase in serum glucose levels with a concomitant reduction in liver glycogen indicating disorders in carbohydrate metabolism due to pesticide induced stress and hence can serve as suitable biomarkers in pesticide toxicity studies.

Topics: Animals; Blood Glucose; Bufonidae; Endosulfan; Glycogen; Insecticides; Liver; Poisoning

The physiological impact of Cd(2+) on Sinopotamon yangtsekiense was evaluated through changes of selected parameters considered as key elements of carbohydrate and protein metabolisms. Crab were exposed to 0.725, 1.45, 2.9mg·L(-1) Cd(2+) for 7, 14 and 21 days. A time- and/or concentration- dependent decrease in muscle glycogen and increase in LDH activity suggested that glycolysis was accelerated during the treatments. Increased protease activity, lowering of FAA and the initially increased and subsequently decreased aminotransferase activities suggest an enhanced protein mobilization during early Cd(2+) exposure followed by a metabolic impairment during late exposure. Decreased hemolymph glucose level was observed in the crabs treated with 2.9mg·L(-1) Cd(2+) for 21d, suggesting an impaired gluconeogenesis. Ammonia level barely changed during the 14d Cd(2+) exposure most likely due to the increased urea and glutamine production; After 1.45 and 2.9mg·L(-1) Cd(2+) treatment for 21d, ammonia was observed increased followed by an exclusive increase in glutamine. Taken together, our results indicate that carbohydrate and protein are mobilized to a varying degree as a compensatory metabolism to response to the energy stress during acute Cd(2+) exposure. As the time lapsed, some symptoms on metabolism obstacle reflect the toxic effect of sublethal Cd(2+).

Topics: Ammonia; Animals; Brachyura; Cadmium; Carbohydrate Metabolism; Dose-Response Relationship, Drug; Fresh Water; Glucose; Glutamine; Glycogen; Heavy Metal Poisoning; Hemolymph; Hepatopancreas; L-Lactate Dehydrogenase; Muscles; Poisoning; Proteins; Transaminases; Water Pollutants, Chemical

Effects in the liver of fatal intoxication with the binary toxin ricin are unclear. We report a robust neutrophil influx into the liver of C57BL/6 mice after lethal parenteral ricin challenge, occurring in peri-portal and centro-lobular hepatic areas within 2 h, followed by the abrupt disappearance of hepatic macrophages/Kupffer cells. Chemokine profiles determined by microarray, ribonuclease protection assays, northern blotting, and enzyme-linked immunosorbent assays showed rapid (2 h) upregulation and persistence of those for neutrophils (CXCL1/KC, CXCL2/MIP-2) and monocytes (CCL2/MCP-1). Red blood cell pooling (8-12 h), loss of hepatocyte glycogen (8-48 h) associated with progressive hypoglycemia, fibrin deposition (24-48 h), and death (72-96 h) followed. Monoclonal antibody to ricin A chain, administered intravenously, blunted hypoglycemia, and abrogated death. This outcome was observed when anti-ricin antibody was given before toxin exposure as well as when administered approximately 10 h after toxin exposure. Targeting antibody to specific amino-acid sequences on the ricin A chain (HAEL and QXXWXXA) was critical to the therapeutic effect. Re-emergence of liver macrophages/Kupffer cells and replenishment of glycogen in previously depleted hepatocytes preceded full recovery of the host. These data identify critical events for liver injury and healing in ricin intoxication, as well as a new means and specific targets for post-exposure therapeutic intervention.

Topics: Animals; Antibodies, Monoclonal; Antibody Specificity; Chemical Warfare Agents; Disease Models, Animal; Epitopes; Glycogen; Hepatocytes; Hypoglycemia; Kupffer Cells; Male; Mice; Oligonucleotide Array Sequence Analysis; Poisoning; Recovery of Function; Ricin

Topics: Ammonia; Animals; Astrocytes; Axons; Brain; Cell Nucleus; Cerebellum; Copper; Glycogen; Hemolysis; Histocytochemistry; Mitochondria; Myelin Sheath; Poisoning; Sheep; Sheep Diseases; Spinal Cord; Time Factors; Urea; Vacuoles

Topics: Acetylcholinesterase; Adenosine Triphosphatases; Administration, Oral; Animals; Chelating Agents; Chick Embryo; Chromium; Chronic Disease; Dogs; Dose-Response Relationship, Drug; Electron Transport Complex IV; Female; Glycogen; Histocytochemistry; Male; Monoamine Oxidase; Myocardium; NADH, NADPH Oxidoreductases; Phosphoric Monoester Hydrolases; Poisoning; Succinate Dehydrogenase; Sulfhydryl Compounds

Topics: Animals; Buffers; Cyclic AMP; Dinitrophenols; Glycogen; Myocardium; Perfusion; Phosphorylase Kinase; Poisoning; Rats; Reserpine; Transferases

Topics: Animals; Cresols; Cytoplasmic Granules; Desmosomes; Fingers; Glycogen; Inclusion Bodies; Mechanoreceptors; Microscopy, Electron; Mitochondria; Organophosphate Poisoning; Pinocytosis; Poisoning; Primates; Schwann Cells

Topics: Adenosine Triphosphate; Alanine; Amino Acids; Aminobutyrates; Ammonia; Animals; Aspartic Acid; Brain; Carbon Isotopes; Cats; Central Nervous System; Chromatography, Paper; Citrates; Colorimetry; Female; Fluorine; Glucose; Glutamates; Glutamine; Glycogen; Kidney; Liver; Lysine; Nerve Tissue Proteins; Poisoning; Rats; Seizures; Spectrophotometry; Spinal Cord

Topics: Desoxycorticosterone; Glycogen; Glycogenolysis; Histamine; Liver; Liver Glycogen; Poisoning

Topics: Carbohydrate Metabolism; Glycogen; Glycogenolysis; Poisoning; Salicylates

Topics: Amino Acids; Animals; Diet, Protein-Restricted; Edible Grain; Fatty Acids; Glycogen; Keto Acids; Liver; Muscles; Oils; Panicum; Poisoning; Poisons; Protein Deficiency; Rats