Izquierdo-Vega JA, Sánchez-Gutiérrez M, Del Razo LM. Decreased in vitro fertility in male rats exposed to fluoride-induced oxidative stress damage and mitochondrial transmembrane potential loss. Toxicol Appl Pharmacol. 2008;230(3):352-7. ISSN: 0041-008X
Fluorosis, caused by drinking water contamination with inorganic fluoride, is a public health problem inmany areas around the world. The aim of the study was to evaluate the effect of environmentally relevantdoses of fluoride on in vitro fertilization (IVF) capacity of spermatozoa, and its relationship to spermatozoamitochondrial transmembrane potential (??m). Male Wistar rats were administered at 5 mg fluoride/kgbody mass/24 h, or deionized water orally for 8 weeks. We evaluated several spermatozoa parameters intreated and untreated rats: i) standard quality analysis, ii) superoxide dismutase (SOD) activity, iii) thegeneration of superoxide anion (O2U), iv) lipid peroxidation concentration, v) ultrastructural analyses ofspermatozoa using transmission electron microscopy, vi) ??m, vii) acrosome reaction, and viii) IVF capability.Spermatozoa from fluoride-treated rats exhibited a significant decrease in SOD activity (~33%), accompaniedwith a significant increase in the generation of O2 U (~40%), a significant decrease in ??m (~33%), and asignificant increase in lipid peroxidation concentration (~50%), relative to spermatozoa from the controlgroup. Consistent with this finding, spermatozoa from fluoride-treated rats exhibited altered plasmaticmembrane. In addition, the percentage of fluoride-treated spermatozoa capable of undergoing the acrosomereaction was decreased relative to control spermatozoa (34 vs. 55%), while the percentage fluoride-treatedspermatozoa capable of oocyte fertilization was also significantly lower than the control group (13 vs. 71%).These observations suggest that subchronic exposure to fluoride causes oxidative stress damage and loss ofmitochondrial transmembrane potential, resulting in reduced fertility.