Abstract
It is known that sodium selenite produces cardiac mitochondrial alterations in vivo and in vitro (Franconi et al. 1980; Dini et al. 1981, 1982). The effect of sodium selenite are reversed by pyruvate administration in vitro and pyruvate treatment also prevented the mitochondrial lesions produced by sodium selenite in vivo. The oxygen consumption of guinea-pig heart isolated mitochondria was studied with glutamate (10 mM) or malate-pyruvate (5 and 10 mM, respectively) as substrates. Sodium selenite (0.1–00.1 mM) significantly reduced (47%–14%) the respiratory control index (RCI) in a dose-dependent manner with glutamate as substrate; on the other hand in the presence of malate-pyruvate no significant difference was observed between the controls and the selenite-treated mitochondria. Moreover, the transaminase and cytochrome-oxidase activities were not changed either in the sodium selenite-treated or the control mitochondria. The above findings suggest that the effects of sodium selenite on mitochondrial oxygen uptake are exerted in a step in which glutamate but not pyruvate-malate are involved.Key wordsSodium seleniteRespiratory functionMitochondriaGuinea pigHeart
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