Passive smoke exposure induces oxidative damage in brains of rat pups: Protective role of diphenyl diselenide

Abstract

The protective effect of diphenyl diselenide, (PhSe)2, on oxidative stress induced by cigarette smoke exposure in brains of rat pups was evaluated. Animals were exposed to passive cigarette smoke (15 min/day) in two different experimental protocols: P1 (1, 2, and 3 cigarettes) and P2 (4, 5, and 6 cigarettes) for 3 weeks. Before each period of smoke exposure, animals received an oral administration of (PhSe)2 (0.5 mg/kg). A number of toxicological parameters in the brain were examined, such as lipid peroxidation, δ-aminolevulinate dehydratase (δ-ALA-D) activity, and components of enzymatic (superoxide dismutase and catalase activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol levels). In P1, smoke exposure induced an inhibition of catalase activity and an increase of ascorbic acid levels. (PhSe)2 treatment was able to protect catalase activity but not ascorbic acid levels. In P2, an augmentation of lipid peroxidation, a reduction of enzymatic and non-enzymatic antioxidant status, and an inhibition of δ-ALA-D activity caused by smoke exposure were found. (PhSe)2 protected the brains of rat pups against oxidative damage induced by smoke exposure. The results are consistent with the antioxidant effect of (PhSe)2 demonstrated by the reduction of oxidative changes caused by smoke exposure in the brains of pups.