Effects of mercury and selenite on delta-aminolevulinate dehydratase activity and on selected oxidative stress parameters in rats.

The present study evaluates the effects of Na(2)SeO(3) and HgCl(2) on kidney and liver of adult rats. In vivo, HgCl(2) (17 micromol/kg, sc) reduced ascorbic acid levels in liver ( approximately 15%), whereas in kidney it reduced ALA-D activity ( approximately 60%) and ascorbic acid levels ( approximately 35%) and increased TBARS content ( approximately 50%). Na(2)SeO(3) (17 micromol/kg, sc) exposure increased the content of nonprotein thiol groups in liver (35-60%) and kidney ( approximately 50-160%), partially prevented mercury-induced ALA-D inhibition in kidney, and completely prevented a mercury-induced increase of TBARS content and decrease of ascorbic acid levels in kidney. In vitro, HgCl(2) and Na(2)SeO(3) inhibited renal and hepatic ALA-D, while HgCl(2) increased TBARS in renal and hepatic tissue preparations. Na(2)SeO(3) increased the rate of glutathione oxidation in vitro. Results indicated that Na(2)SeO(3) protected against HgCl(2) effects in vivo (prevention of mercury interaction with thiol groups and of mercury-induced oxidative damage). In vitro, Na(2)SeO(3) did not prevent mercury effects, but potentiated ALA-D inhibition by mercury, probably due to its ability to oxidize thiol groups.