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

The present study evaluates the effects of Na2SeO3 and HgCl2 on kidney and liver of adult rats. In vivo, HgCl2 (17 μmol/kg, sc) reduced ascorbic acid levels in liver ( 15%), whereas in kidney it reduced ALA-D activity ( 60%) and ascorbic acid levels ( 35%) and increased TBARS content ( 50%). Na2SeO3 (17 μmol/kg, sc) exposure increased the content of nonprotein thiol groups in liver (35–60%) and kidney ( 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, HgCl2 and Na2SeO3 inhibited renal and hepatic ALA-D, while HgCl2 increased TBARS in renal and hepatic tissue preparations. Na2SeO3 increased the rate of glutathione oxidation in vitro. Results indicated that Na2SeO3 protected against HgCl2 effects in vivo (prevention of mercury interaction with thiol groups and of mercury-induced oxidative damage). In vitro, Na2SeO3 did not prevent mercury effects, but potentiated ALA-D inhibition by mercury, probably due to its ability to oxidize thiol groups.