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Mercury intoxication has been associated with male reproductive toxicity in experimental animals and mercury may have the potential to produce adverse effects on fertility in men. Vitamin E may protect against toxic effects of mercury in the liver and other tissues. To investigate the protective role of vitamin E against mercuric chloride toxicity for the testis, epididymis, and vas deferens of adult male mice, animals were treated with either mercuric chloride 1.25 mg/kg/day, vitamin E 2 mg/kg/kg, or a combination of the two treatments. Control animals were treated with water. Treatments were administered by daily gavage for 45 days. An additional group of animals treated with mercuric chloride were permitted to recover for 45 days after mercuric chloride treatments. Parameters studied included serum testosterone, epididymal sperm count, motility, and morphology, epididymal and vas deferens adenosine triphosphatase (ATPase), phosphorylase, sialic acid, glycogen and protein, testicular succinate dehydrogenase (SDH), phosphatases, cholesterol, ascorbic acid, and glutathione. Fertility was evaluated by sperm positive vaginal smears after overnight cohabitation with a female. Mercuric chloride produced a reduction in epididymal sperm count, sperm motility, and sperm viability, and there were no sperm-positive smears in this group. Biochemical tests from the male reproductive organs were also altered by mercuric chloride treatment. Coadministration of vitamin E with mercuric chloride prevented the changes in sperm and biochemical parameters and was associated with control rates of sperm positive smears after cohabitation. Animals given vitamin E with mercuric chloride also had lower concentrations of mercury in the testis, epididimyis, and vas deferens. Permitting animals to recover for 45 days after mercuric chloride treatment resulted in partial recovery of sperm and biochemical parameters. Vitamin E cotreatment has a protective role against mercury-induced male reproductive toxicity.

Effects of oral administration of mercuric chloride (HgCl 2 ,1.25 mg/kg) daily for 30 d on the mouse testis, vas deferens, epididymis, and cauda epididymal sperm were investigated. Testis, vas deferens, and epididymis functions were evaluated with respect to sperm count, motility, and viability, and biochemical tests, including succinate dehydrogenase (SDH), adenosine triphosphatase, sialic acid, protein, cholesterol, and glycogen levels in these tissue. Sperm morphology and sperm nuclear integrity were evaluated with standard staining methods. Treatment did not affect whole body and tissue weights. Sperm parameters and fertility were reduced by HgCl 2 and most of the biochemical parameters declined. Morphologic histologie alterations were also observed in the tissues studied. All parameters partially recovered after withdrawal of HgCl 2 for 45 d.

Effects of diethylstilbestrol (DES) treatment (30 daily i.m. injections) in reproductive function in the male rat were investigated. These functions were evaluated with sperm counts, motility, fertility, morphology, serum testosterone, and a number of biochemical tests in rat epididymis and vasa deferentia. DES treatment resulted in a 15% loss of body weight and a 60 to 90% loss of weight of testes, epididymis, and vas deferens. Sperm parameters and fertility were reduced to nil by DES treatment. Likewise, the majority of the biochemical measures were severely depressed by the DES treatment. In general, the measured parameters were less affected or recovered with either testosterone cotreatment or 60 days of recovery, showing the role of androgen in maintaining functional integrity and metabolism. However, sperm parameters and fertility did not recover with testosterone cotreatment, which differs from withdrawal of treatment.

A single microdose (50 μg/50 μL) injection of sodium fluoride (NaF) into the vasa deferentia of adult male albino rats ( Rattus norvegicus ) caused arrest of spermatogenesis and absence of spermatozoa in the lumina of the seminiferous tubules of the testes, which consequently led to a decline in the sperm count in the caudae epididymides. Scanning electron microscopy of cauda and vas deferens sperm revealed deflagellation and tail abnormalities. This is probably related to the alterations in the internal milieu of these organs which rendered the spermatozoa immotile and consequently caused fertility impairment in the experimental animals. Thus microdoses of sodium fluoride were found to affect reproductive function and fertility rate.