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 HgCl(2) toxicity. Rats were injected with HgCl(2) (0 or 17 micromol/kg, sc) 6 h after organoselenium compounds had been injected (0 or 50 micromol/kg, sc). In vivo, HgCl(2) inhibited renal ALA-D activity ( approximately 48%), increased TBARS level in kidney ( approximately 52%) and reduced the hepatic content of non-protein thiol groups ( approximately 40%), but organoselenium compounds did not prevent such effects. SeCis, per se, increased renal TBARS level ( approximately 42%), while AASe increased hepatic content of ascorbic acid ( approximately 38%). In vitro, renal and hepatic ALA-D activity was inhibited by HgCl(2) (>or=25 microM), ebselen (>or=12 microM) and SeCis (>or=4 microM). HgCl(2) (400 microM) 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.