glycogen and Cadmium-Poisoning

Topics: Animals; Behavior, Animal; Cadmium Poisoning; Color Perception; Eye Abnormalities; Fishes; Glycogen; Liver Glycogen; Muscles

The effects of acute (24 h) and chronic (90 days) cadmium (Cd) poisoning on blood and tissue metabolite levels of a teleost, Puntius conchonius were studied. Significant hyperglycemia with an increment in liver, kidney and ovary cholesterol occurred during acute Cd poisoning. By contrast, an enduring hypoglycemia and diminished levels of tissue cholesterol manifested the chronically intoxicated fish. Both acute and chronic Cd poisoning, however, caused marked hypocholesterolemia, glycogenolysis in liver and brain, and a concomitant rise in myocardium glycogen concentration. Testes cholesterol was found to be depleted after both acute and chronic (60 days) Cd poisoning.

Topics: Animals; Blood Glucose; Brain; Cadmium Poisoning; Cholesterol; Female; Fishes; Glycogen; Kidney; Liver; Ovary

After the long-term exposure to cadmium chloride in drinking water, the Wistar rats developed peripheral polyneuropathy. The main lesion was of myelin degeneration. Ultrastructural examination of the roots and sciatic nerves revealed segmental demyelination beginning from the node of Ranvier. There was the active autophagocytosis of Schwann cells which contained a number of myelin remnants and dense bodies. There was, on the other hand, the evidence of remyelination with toxic damage, in which the thinner myelin sheaths and abnormal myelinations were observed with increase of Schwann cells containing rich ribosomes. Axoplasmic changes were minimal, but consisted of accumulation of glycogen particles which very often produced glycogenosomes in characteristic appearance with axoplasmal dysfunction.

Topics: Animals; Axons; Cadmium Poisoning; Chronic Disease; Demyelinating Diseases; Glycogen; Microscopy, Electron; Myelin Sheath; Peripheral Nervous System Diseases; Phagocytosis; Ranvier's Nodes; Rats; Ribosomes; Schwann Cells; Sciatic Nerve; Spinal Nerve Roots