A REVIEW OF EXPERIMENTAL METHYLMERCURY TOXICITY IN RATS - NEUROPATHOLOGY AND EVIDENCE FOR APOPTOSIS

As an animal model for examining the pathogenicity of human organic me rcury intoxication, rats have been used for the reproduction of human neurologic diseases. Rats experimentally exposed to methylmercury chlo ride showed clinical signs of neurologic dysfunction characterized by ataxic behavior. Neuropathology of the diseased animals consisted of l esions such as: (a) degeneration of the peripheral nerve and sensory r oot nerve with preservation of the motor root nerve; (b) degeneration of the posterior funiculus of the spinal cord; and (c) degeneration of cerebellar granule cells with preservation of Purkinje cells. These f indings suggest the human neuropathology of this toxicity. The degener ation was characterized by nerve fiber damage or neuronal cell death a ccompanied by astrocytic gliosis and activated macrophages or microgli as. For the cerebellar granule cells, the mechanism of neuronal cell d eath was shown to be apoptosis. This fact was verified by histologic a nd ultrastructural findings as well as by in situ nick-end labeling an d electrophoretic methods. Evidence of apoptosis involvement in cerebe llar degeneration would provide a new viewpoint from which to analyze the selected degeneration of the nervous system in neurotoxicology.