NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of a-tocopherol

Fluorosis, caused by drinkingwater contaminated with inorganic fluoride, is a public health problem inmany areasaround theworld. The aim of this studywas to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidasein relationship to fluoride. Four experimental groups of maleWistar ratswere administered with deionizedwater, NaF, at a doseequivalent to 5 mg fluoride kg-1 per 24 h, NaF plus 20 mg kg-1 per 24 h a-tocopherol, or a-tocopherol alone for 60 days. Weevaluated several spermatozoa parameters in the four groups: standard quality analysis, superoxide dismutase (SOD) activity,the generation of reactive oxygen species (ROS), NADPH oxidase activity, TBARS formation, ultrastructural analyses ofspermatozoa using transmission electron microscopy and in vitro fertilization (IVF) capacity.After 60 days of treatment, urinaryexcretion of fluoridewas not modified by a-tocopherol. Spermatozoa fromfluoride-treated rats exhibited a significant increasein the generation of ROS, accompanied by a significant increase in NADPH oxidase activity. The increase in ROS generationwassignificantly diminished by diphenylene iodonium, an inhibitor of NADPH oxidase activity. In contrast, a decrease in thegeneration of ROS, an increase in SOD activity and the prevention of TBARS formation process were observed in spermatozoaof rats exposed to fluoride plus a-tocopherol. Finally, a-tocopherol treatment prevented the IVF incapacity observed in thespermatozoa from fluoride-treated rats. These results suggest that NADPH oxidase participates in the oxidative stress damagecaused by subchronic exposure to fluoride. Copyright 2010 JohnWiley & Sons, Ltd.