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NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of α ‐tocopherol
Author(s) -
IzquierdoVega Jeannett A.,
SánchezGutiérrez Manuel,
Del Razo Luz María
Publication year - 2011
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1600
Subject(s) - tbars , oxidative stress , fluoride , chemistry , nadph oxidase , reactive oxygen species , superoxide dismutase , tocopherol , biochemistry , superoxide , antioxidant , andrology , pharmacology , enzyme , lipid peroxidation , vitamin e , biology , medicine , inorganic chemistry
Fluorosis, caused by drinking water contaminated with inorganic fluoride, is a public health problem in many areas around the world. The aim of this study was to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. Four experimental groups of male Wistar rats were administered with deionized water, NaF, at a dose equivalent to 5 mg fluoride kg −1 per 24 h, NaF plus 20 mg kg −1 per 24 h α ‐tocopherol, or α ‐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 fluoride was not modified by α ‐tocopherol. Spermatozoa from fluoride‐treated rats exhibited a significant increase in the generation of ROS, accompanied by a significant increase in NADPH oxidase activity. The increase in ROS generation was 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 α ‐tocopherol. Finally, α ‐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 John Wiley & Sons, Ltd.