Aluminum accumulation induced testicular oxidative stress and altered selenium metabolism in mice.

Present work was carried out to investigate how testicular selenium (Se) metabolisms respond to oxidative stress induced by aluminum (Al). Mice were intraperitoneally exposed to 0, 7, or 35mg Al/kg/d for 14 days (CNL, LAL and HAL groups). Al administration significantly increased Al, reactive oxygen radical and malondialdehyde (MDA) levels, as well as decreased glutathione peroxidase (GPx) and glutathione reductase (GR) activities in serum and testes. The serum concentrations of Se were remarkably lower at LAL and HAL groups compared to the controls, whereas the testicular Se levels significantly reduced only in the HAL group. In addition, RT-PCR analysis revealed an increased testicular selenoprotein P (SelP) expression by Al treatment. Western blot analysis showed increased levels of SelP protein expression in the LAL group, but the expression levels were significantly reduced in HAL group. It was suggested that altered metabolism of Se, further stimulated testicular SelP transcription that may compensate for the loss of SelP protein resulted from Al-induced oxidative damage.