The use of the trimethyltin model of CNS neurotoxicity to study biochemical indices of neuropathological change in the rat.
Trimethyltin (TMT)-induced CNS neurotoxicity in the rat was used to study biochemical indices of neuropathological change. The parameters measured were DNA and the lysosomal enzymes beta-glucuronidase and beta-galactosidase. Three brain regions were investigated, hippocampus, medulla and cerebellum. Rats received 4 mg/kg TMT weekly for a maximum of 5 weeks. The largest changes were found in the hippocampus, with smaller changes in medulla and no changes in the cerebellum. In the hippocampus the beta-glucuronidase activity was increased after three weeks to a maximum of 264% of the mean control value, while the beta-galactosidase activity was reduced to 87% of the control value. The lysosomal enzyme changes were attributed to processes of astrocytic and microglial hypertrophy and neuronal cell loss. The neuronal cell loss was further substantiated by the gradual reduction in the level of DNA in the hippocampus. It was concluded that the TMT model of CNS neurotoxicity in the rat hippocampus was a useful tool for studying biochemical indices of neuropathological change.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002493:Central Nervous System Diseases / Q000139:chemically induced* / Q000378:metabolism; D002531:Cerebellum / Q000378:metabolism; D004247:DNA / Q000032:analysis; D005966:Glucuronidase / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D008526:Medulla Oblongata / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D014220:Trialkyltin Compounds / Q000494:pharmacology*; D014298:Trimethyltin Compounds / Q000494:pharmacology*; D001616:beta-Galactosidase / Q000378:metabolism; D001617:beta-Glucosidase / Q000378:metabolism
D014220:Trialkyltin Compounds; D014298:Trimethyltin Compounds; D004247:DNA; D001617:beta-Glucosidase; D001616:beta-Galactosidase; D005966:Glucuronidase