Abstract
Previous studies in humans and animals have suggested that lead (Pb) may increase the expression of amyloid precursor protein (APP) and accumulation of amyloid β protein (Aβ). Our previous studies have revealed that selenium (Se) can partially improve memory deficits induced by Pb exposure. In this study we sought to investigate the effect of Pb and Se on the endogenous expression of APP, Aβ40 and Bcl-2 family proteins. In vitro, the protein levels of APP and Aβ significantly decreased in SH-SY5Y and PC12 cells co-incubated with Pb-acetate and selenomethionine (SeMet) for 48h, compared with cells treated with Pb-acetate alone. Furthermore, these reductions induced by Se appeared to be concentration-dependent. In Wistar rats, we observed that the mRNA and protein levels of APP, the protein level of Bax, and the ratio of Bax/Bcl-2 protein significantly increased after Pb treatment at embryonic stage and in neonates. These increases were significantly reversed by the treatment of Se. Taken together, our results suggest that Se can attenuate the alterations in APP expression and Aβ production as well as Bcl-2 family proteins induced by lead exposure in cells and in animals.
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