Arsenic-induced changes in optic tectal histoarchitecture and acetylcholinesterase-acetylcholine profile in Channa punctatus: amelioration by selenium.

Fish (Channa punctatus Bloch) were exposed in vivo for 14 days to non-lethal doses of As2O3 (10% LC50 and 5% LC50). Several endpoints related to histoarchitectural and acetylcholine-acetylcholinesterase (ACh-AChE) profile in the optic tectum were evaluated. Histological examination showed aggregated, disorganized and necrotic cells with irregular outlines in the different layers of optic tectum in the As-treated fish. The histopathological changes were more pronounced on day 7 than on other days and the damage was found to recover on day 14. ACh content and AChE activity demonstrated the usual inverse trend. Arsenic treatment was associated with a dose-dependent increase in AChE activity on day 1, a decrease on day 2 and reactivation on day 7, returning to the basal level on day 14. In vitro inhibition kinetics were set up to determine I50 (35 microM) concentration of As2O3. The ameliorative potential of selenium on arsenic-mediated inhibition of AChE revealed a positive role of Se, especially when Se preceded As2O3 treatment, either in vitro or in vivo.