Renal and hepatic ALA-D activity and selected oxidative stress parameters of rats exposed to inorganic mercury and organoselenium compounds

This paper evaluates the ability of organoselenium compounds [ebselen, selenocystine N-ethyl-carbamate (SeCis), bis-4-isopropyl-2-oxazolinyl phenyl diselenide (AASe)] to prevent HgCl2 toxicity. Rats were injected with HgCl2 (0 or 17 μmol/kg, sc) 6 h after organoselenium compounds had been injected (0 or 50 μmol/kg, sc). In vivo, HgCl2 inhibited renal ALA-D activity (∼48%), increased TBARS level in kidney (∼52%) and reduced the hepatic content of non-protein thiol groups (∼40%), but organoselenium compounds did not prevent such effects. SeCis, per se, increased renal TBARS level (∼42%), while AASe increased hepatic content of ascorbic acid (∼38%). In vitro, renal and hepatic ALA-D activity was inhibited by HgCl2 (⩾25 μm), ebselen (⩾12 μm) and SeCis (⩾4 μm). HgCl2 (400 μm) significantly increased TBARS production in renal and hepatic tissue preparations in vitro, and this effect was completely or partially prevented by organoselenium compounds. Ebselen exhibited thiol peroxidase activity in our assay conditions, while SeCis exhibited thiol-oxidizing properties regardless of the presence of peroxide. AASe had no effect on thiol oxidation. Results suggest that organoselenium compounds could not prevent mercury toxicity in vivo. The protective effect of these compounds against mercury-induced increase of TBARS production in vitro is probably related to an antioxidant action rather than to mercury binding.