Article ID Journal Published Year Pages File Type
2594622 Reproductive Toxicology 2006 7 Pages PDF
Abstract
Fluoride contamination of drinking water can disrupt male gametogenesis and steroidogenesis and induce testicular oxidative stress. Treatment of rats with sodium fluoride at the dose of 20 mg/kg/day for 28 days resulted in significant diminution of testicular Δ5,3β-hydroxysteroid dehydrogenase (HSD) and 17β-hydroxysteroid dehydrogenase (HSD) activities and low plasma levels of testosterone, follicular stimulating hormone (FSH) and leutinizing hormone (LH). Spermatogenesis inhibited after sodium fluoride treatment has been assessed here by the quantification of different generation of germ cells like spermatogonia A (ASg), preleptotene spermatocyte (PLSc), midpachytene spermatocyte (MPSc) and step 7 spermatid (7Sd) at stage VII of seminiferous epithelial cycle. Furthermore, fluoride treatment was associated with low activities of testicular, prostatic and epididymal catalase (CAT), superoxide dismutase (SOD) and peroxidase along with elevation of malondialdehyde (MDA) and conjugated dienes (CD) in those tissues. Co-administration of calcium and Vitamin-E with fluoride resulted in a significant recovery from testicular disorders and oxidative stress in the testis and male accessory sex organs. The results of this study demonstrate that fluoride exposure, at the dose available in drinking water in contaminated areas, led to inhibition of testicular gametogenesis and steroidogenesis in association with oxidative stress in the testis and male accessory sex organs, which are protected significantly by dietary agents like Vitamin-E and calcium.
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Life Sciences Environmental Science Health, Toxicology and Mutagenesis
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