Chemico-Biological Interactions 165 (2007) 87–98 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 Robson Luiz Puntel, Daniel Henrique Roos, M´ arcio Weber Paix˜ ao, Ant ˆ onio Luiz Braga, Gilson Zeni, Cristina Wayne Nogueira, Joao Batista Teixeira Rocha ∗ Departamento de Qu´ ımica, Centro de Ciˆ encias Naturais e Exatas, Universidade Federal de Santa Maria, Campus UFSM, Santa Maria, RS 97105-900, Brazil Received 31 July 2006; received in revised form 3 November 2006; accepted 9 November 2006 Available online 23 November 2006 Abstract 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 Fe 2+ plus H 2 O 2 , whereas at 20 mmol/l it significantly prevents its degradation. Oxalate (up to 4 mmol/l) did not alter iron (10 mol/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 4mmol/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. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Oxalate; Diphenyl diselenide; Diphenyl ditelluride; Iron; TBARS 1. Introduction Hyperoxaluria is one of the main risk factors of human idiopathic calcium oxalate disease. Oxalate, the major stone-forming constituent is known to induce ∗ Corresponding author. Tel.: +55 21 3220 8140; fax: +55 21 3220 8978. E-mail address: jbtrocha@yahoo.com.br (J.B.T. Rocha). lipid peroxidation, which causes disruption of the cellular membrane integrity [1,2]. Oxidative stress may be caused by increased concentrations of free oxalate ions or by insoluble calcium oxalate interacting directly with renal epithelial cells, or may originate from other inflammatory event [3]. Exposure to high concentrations of oxalate can induce oxidative stress, as shown by (i) increased lipid peroxidation (thiobarbituric acid reactive species-TBARS) [4,5], (ii) decreased reduced glutathione concentrations [6], (iii) increase in free 0009-2797/$ – see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.cbi.2006.11.003