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 areas around theworld. The aim of this studywas to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. Four experimental groups of maleWistar ratswere administered with deionizedwater, NaF, at a dose equivalent 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. We evaluated 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 of spermatozoa using transmission electron microscopy and in vitro fertilization (IVF) capacity.After 60 days of treatment, urinary excretion of fluoridewas not modified by a-tocopherol. Spermatozoa fromfluoride-treated rats exhibited a significant increase in the generation of ROS, accompanied by a significant increase in NADPH oxidase activity. The increase in ROS generationwas significantly diminished by diphenylene iodonium, an inhibitor of NADPH oxidase activity. In contrast, a decrease in the generation of ROS, an increase in SOD activity and the prevention of TBARS formation process were observed in spermatozoa of rats exposed to fluoride plus a-tocopherol. Finally, a-tocopherol treatment prevented the IVF incapacity observed in the spermatozoa from fluoride-treated rats. These results suggest that NADPH oxidase participates in the oxidative stress damage caused by subchronic exposure to fluoride. Copyright 2010 JohnWiley & Sons, Ltd.