Diphenyl diselenide reduces temporarily hyperglycemia: possible relationship with oxidative stress.

This study was designed to determine the effect of diphenyl diselenide and ebselen, synthetic organoselenium compounds with antioxidant properties, in diabetic rats. Diabetes was induced by the administration of streptozotocin (STZ) (45mg/kg, intravenous). In experimental trials, diphenyl diselenide, but not ebselen, caused a significant reduction in blood glucose levels of STZ-treated rats. This effect of diphenyl diselenide was accompanied by a reduction in the levels of glycated proteins. Diphenyl diselenide ameliorate superoxide dismutase activity (liver and erythrocytes) and Vitamin C levels (liver, kidney and blood), which were decreased in STZ-treated rats. In normal rats, diphenyl diselenide caused per se an increase in hepatic, renal and blood GSH levels. Similarly, treatment with diphenyl diselenide restored hepatic and renal GSH levels in STZ-treated rats. TBARS and protein carbonyl levels were not modified by STZ and/or diphenyl diselenide and ebselen treatments. Our findings suggest that diphenyl diselenide can be considered an anti-diabetogenic agent by exhibiting anti-hyperglycemic and antioxidant properties.

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.