An ultrastructural study of chronic cadmium chloride-induced neuropathy.
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.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D002105:Cadmium Poisoning / Q000473:pathology*; D002908:Chronic Disease; D003711:Demyelinating Diseases / Q000473:pathology; D006003:Glycogen / Q000032:analysis; D008854:Microscopy, Electron; D009186:Myelin Sheath / Q000648:ultrastructure; D010523:Peripheral Nervous System Diseases / Q000473:pathology*; D010587:Phagocytosis; D011901:Ranvier's Nodes / Q000648:ultrastructure; D051381:Rats; D012270:Ribosomes / Q000648:ultrastructure; D012583:Schwann Cells / Q000648:ultrastructure; D012584:Sciatic Nerve / Q000648:ultrastructure; D013126:Spinal Nerve Roots / Q000648:ultrastructure
D006003:Glycogen