Oxalate modulates thiobarbituric acid reactive species (TBARS) production in supernatants of homogenates from rat brain, liver and kidney: Effect of diphenyl diselenide and diphenyl ditelluride

The aim of this paper was to investigate the mechanism(s) involved in the sodium oxalate pro-oxidative activity in vitro and the potential protection by diphenyl diselenide ((PhSe)2) and diphenyl ditelluride ((PhTe)2) using supernatants of homogenates from brain, liver and kidney. Oxalate causes a significant increase in the TBARS (thiobarbituric acid reactive species) production up to 4 mmol/l and it had antioxidant activity from 8 to 16 mmol/l in the brain and liver. Oxalate had no effect in kidney homogenates. The difference among tissues may be related to the formation of insoluble crystal of oxalate in kidney, but not in liver and brain homogenates. (PhSe)2 and (PhTe)2 reduced both basal and oxalate-induced TBARS in rat brain homogenates, whereas in liver homogenates they were antioxidant only on oxalate-induced TBARS production. (PhSe)2 showed a modest effect on renal TBARS production, whereas (PhTe)2 did not modulate TBARS in kidney preparations. Oxalate at 2 mmol/l did not change deoxyribose degradation induced by Fe2+ plus H2O2, whereas at 20 mmol/l it significantly prevents its degradation. Oxalate (up to 4 mmol/l) did not alter iron (10 μmol/l)-induced TBARS production in the brain preparations, whereas at 8 mmol/l onwards it prevents iron effect. In liver preparations, oxalate amplifies iron pro-oxidant activity up to 4 mmol/l, preventing iron-induced TBARS production at 16 mmol/l onwards. These results support the antioxidant effect of organochalcogens against oxalate-induced TBARS production. In addition, our results suggest that oxalate pro- and antioxidant activity in vitro could be related to its interactions with iron ions.