CONICET | Buscador de Institutos y Recursos Humanos

The hypothesis of this work was that radical generation after exposureto As may contribute to its toxic effects in the brain tissues. Oxidativestatus of brain was studied, both using ex vivo and in vivo protocols ofexposure to the toxic. The generation rate of lipid radicals (LR●), andascorbyl radical (A●) content, were measured by Electron ParamagneticResonance (EPR). In the ex vivo model control brain homogenates wereexposed to As, and a 2-fold increase was detected in the LR● generationrate, with no changes in A● radical content. A significant decrease of33% and 30% in the content of glutathione (GSH) was measured afterexposure to 3.3 and 4.0 pmol As/mg FW, respectively. In the in vivomodel, As was ip injected to rats and the rate of generation of LR● byhomogenates of brain tissue, was increased by 81 and 122%, ascompared to control animals after the injection of 3.0 and 5.8 mgAs/kg, respectively. Neither GSH, nor -tocopherol (-T) norascorbate (AH-) content was affected in As-treated rats, as compared tothe values from control animals. The LR●/α-T content ratio wassignificantly increased in As-treated animals as compared to controlbrains. The A●/AH− content ratio was not affected by As exposure. Thecontent of total Fe showed non-significant differences between controland rat brains after 24 h of As administration. The data presented hereshowed new evidence on the generation of specific radical species byAs treatment employing EPR methodologies in both, ex vivo and invivo models. The data suggested the triggering of different pathwaysleading to some reactive species generation may occur accordingly tothe via As reaches the brain, even when the same concentration of thetoxic was achieved by the tissues.