Methylated tin toxicity a reappraisal using rodents models.

Abstract

Trimethyltin-induced intoxication has a great impact on human health due to the widespread occurrence of methyltin compounds. Acute TMT intoxication in humans leads to a variety of neurological symptoms which involve primarily the limbic system. In the present review we summarized the neuromorphological correlates of this neurological syndrome extending the analysis to various extra-limbic regions and detailing the fine ultrastructure of TMT-induced neuronal alterations. In order to comprehend the pathophysiology of TMT-induced neuronal damage we analysed the various experimental models of TMT-induced neurotoxicity. When comparing various animal species, it seems that the variety of neuropathological correlates are not related to species difference in the sensitivity to TMT toxicity but to a different susceptibility to secondary effects produced by TMT. In fact, apart from a primary neurotoxic damage induced by TMT at neuronal level, this compound promotes the onset of limbic and generalized seizures, which in turn add a secondary damage to that induced immediately by TMT. Thus, the different neuropathology observed in different animal species is produced mainly by a different sensitivity to epilepsy-induced brain damage.