Oxidative balance in brain after exposure to arsenic in ex vivo and in vivo models

Abstract

The hypothesis of this work was that radical generation after exposure<br />to As may contribute to its toxic effects in the brain tissues. Oxidative<br />status of brain was studied, both using ex vivo and in vivo protocols of<br />exposure to the toxic. The generation rate of lipid radicals (LR●), and<br />ascorbyl radical (A●) content, were measured by Electron Paramagnetic<br />Resonance (EPR). In the ex vivo model control brain homogenates were<br />exposed to As, and a 2-fold increase was detected in the LR● generation<br />rate, with no changes in A● radical content. A significant decrease of<br />33% and 30% in the content of glutathione (GSH) was measured after<br />exposure to 3.3 and 4.0 pmol As/mg FW, respectively. In the in vivo<br />model, As was ip injected to rats and the rate of generation of LR● by<br />homogenates of brain tissue, was increased by 81 and 122%, as<br />compared to control animals after the injection of 3.0 and 5.8 mg<br />As/kg, respectively. Neither GSH, nor -tocopherol (-T) nor<br />ascorbate (AH-) content was affected in As-treated rats, as compared to<br />the values from control animals. The LR●/α-T content ratio was<br />significantly increased in As-treated animals as compared to control<br />brains. The A●/AH− content ratio was not affected by As exposure. The<br />content of total Fe showed non-significant differences between control<br />and rat brains after 24 h of As administration. The data presented here<br />showed new evidence on the generation of specific radical species by<br />As treatment employing EPR methodologies in both, ex vivo and in<br />vivo models. The data suggested the triggering of different pathways<br />leading to some reactive species generation may occur accordingly to<br />the via As reaches the brain, even when the same concentration of the<br />toxic was achieved by the tissues.