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UK Against Fluoridation

Monday, July 16, 2012

To study the effect of vitamin D and E on sodium-fluoride-induced toxicity in reproductive functions of male rabbits

How to cite this
Kumar N, Sood S, Arora B, Singh M, Beena, Roy PS. To study the effect of vitamin D and E on sodium-fluoride-induced toxicity in reproductive functions of male rabbits. Toxicol Int [serial online] 2012 [cited 2012 Jul 16];19:182-7. Available from: http://www.toxicologyinternational.com/text.asp?2012/19/2/182/97220
Introduction
Fluorosis is an endemic public health problem in many nations around the world. The World Health Organization (WHO) guideline is that 1.5 ppm of fluoride is the desirable upper limit in drinking water and the recommended levels are 0.5 to 0.8 mg/L. [1] Extensive data on skeletal fluorosis are available. However, the effect of fluoride on the structure and metabolism of several soft tissues has been reported recently and convincing evidence from fluorosis patient is now available to demonstrate the damage or involvement of human spermatozoa. [2] Chinoy and Sequeira reported that sodium fluoride treatment in mice caused alteration in histology of reproductive organs, morphology of sperm, and induced biochemical changes. [3],[4] In fluoride-treated male rats there was decrease in sperm motility. [5] In an Indian study, infertility was reported among married men in a highly endemic area with fluoride concentration up to 38.5 mg/L. [6] Sodium fluoride treatment (20 mg/kg/day for 29 days) results a significant diminution of relative wet weight of the testis, prostate, and seminal vesicle, without alteration in the body weight. [7] Susheela and Kumar have shown that chronic fluoride toxicity caused regression of seminiferous tubule and cessation of the spermatogenesis in the rabbit. [8] Fluoride treatment leads to oxidative stress as indicated by an increased level of conjugated dienes in the testis, epididymis, and epididymal sperm with respect to control. [7] Vitamin D (vit D) hormone plays an important role in reproduction. [9],[10],[11] Sood et al. suggested that deficiency of vitamin D produces retardation of spermatogenesis due to disturbances in sertoli cell functions, and these changes are reversible and can be corrected by supplementing an optimal dose of vitamin D. [12] Vitamin E (vit E) is believed to exert its protective effect at the cellular - molecular level, primarily through destruction of cell damaging free radical oxygen species. [13] Chinoy and Sharma reported that the supplementation of vitamin D and E during the withdrawal period of sodium-fluoride-treated mice was found to be very beneficial in recovery of all sodium-fluoride-induced effects on reproductive functions and fertility. The extent of recovery was more pronounced with vitamin E as compared to vitamin D and was most significant with the combined treatment. However, not many studies are available to show the effect of vitamin D and E in fluorosis. [14]

Considering that fluorosis is a public health issue and the very fact that the fluoride exposure has a definite effect on reproduction. The following study was planned to observe the effect of fluoride on the sperm count, motility, and histology of testis and to study the ameliorative effect, if any of vitamin D and E either alone or in combination.

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