Efeito dos organocalcogênios sobre a atividade da enzima δ-ALA-D sanguínea: estudos in vitro e em humanos expostos ocupacionalmente a estes compostos

Abstract

Organochalcogens are important intermediates and the main applied reagents in organic synthesis, which can increase human exposure risk to these chemicals in the workplace. Since, the erythrocytic δ-ALA-D activity could be an important indicator of toxicity this report investigated the organochalcogens effects on blood δ-ALA-D in vitro and determined δ-ALAD activity on human occupationally exposed to organochalcogens. The acute tixicity of organochalcogens on erythrocytic δ-ALA-D activity, in mice, was also investigated. δ-ALA-D activity was assayed according to the method of Berlin & Schaller (1974) with some modifications. Diphenyl ditelluride, diphenyl diselenide and Ebselen inhibited in a concentration-dependent manner δ-ALA-D activity from human erythrocytes. Dithiothreitol (DTT), the hydrophobic SH-reducing agent, was able to reactivate and to protect inhibited δ-ALA-D. The administration of diphenyl diselenide (200 μmol/kg) and diphenyl ditelluride (150 μmol/kg) in a toxic amount inhibited the erythrocytic δ-ALA-D activity on mice. Otherwise, the human occupationally exposed to organochalcogens did not increase selenium levels, from these findings we can not affirm that human δ-ALA-D was a target for organochalcogens ex vivo. In addition δ-ALA-D was a target toxicity from organochalcogens, in vitro. But, mice erytrocytes δ-ALA-D was a target for organochalcogens tested ex vivo.