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The present study investigated the long-term effects of prenatal betamethasone exposure on sperm quality and count, fertility and plasma testosterone levels in adult male rats. Pregnant rats received 0.1 mg kg(-1) betamethasone on Days 12, 13, 18 and 19 of pregnancy. This treatment impaired sperm quality, sperm production, fertility and plasma testosterone levels in adult male offspring compared to the control group. Thus, the results of the present study indicate that the long-term effects of prenatal betamethasone exposure may be deleterious to offspring. The consequent decrease in testosterone production during adulthood, in association with damaged semen parameters, may explain for the observed decrease in the capacity of adult male offspring to themselves generate viable descendants.

Sibutramine is an inhibitor of norepinephrine and 5-HT reuptake largely used in the management of obesity. Although a fairly safe drug, postmarketing adverse effects of sibutramine were reported including abnormal ejaculation in men. This study investigates the effects of sibutramine on ejaculation and vas deferens and seminal vesicle contractility. Adult male rats received sibutramine (5; 20; or 50 mg kg(-1), ip) and after 60 min were exposed to receptive females for determination of ejaculation parameters. The vasa deferentia and seminal vesicles of untreated rats were mounted in isolated organ baths for recording of isometric contractions and HEK293 cells loaded with fluorescent calcium indicator were used to measure intracellular Ca(2+) transients. Sibutramine 5 and 20 mg kg(-1) reduced ejaculation latency whereas 50 mg kg(-1) increased ejaculation latency. Sibutramine 3 to 30 microM greatly increased the sensitivity of the seminal vesicle and vas deferens to norepinephrine, but at concentrations higher than 10 microM there were striking depressions of maximal contractions induced by norepinephrine, carbachol and CaCl(2). In HEK293 cells, sibutramine 10 to 100 microM inhibited intracellular Ca(2+) transients induced by carbachol. Depending on the doses, sibutramine either facilitates or inhibits ejaculation. Apart from its actions in the central nervous system, facilitation of ejaculation may result from augmented sensitivity of smooth muscles to norepinephrine while reductions of intracellular Ca(2+) may be involved in the delayed ejaculation observed with high doses of sibutramine.

The aim of this study was to investigate the potential estrogenic activity of fenvalerate by examining reproductive and fertility capabilities in Wistar rats. Adult male animals were treated for 30 d with 20 or 40 mg/kg/d fenvalerate or corn oil (vehicle) by oral gavage. Further, a possible estrogenic activity of fenvalerate (0.4, 1, 4, 8, or 40 mg/kg) was tested after a 3-d treatment of immature female rats using the uterotrophic assay. Exposure to the higher dose of fenvalerate was toxic to testis and epididymis as shown by a decrease in the absolute weights and sperm counts in both organs. Although the sperm counts were reduced, the fertility and sexual behavior were similar in control rats and rats treated with 40 mg/kg pesticide. Fenvalerate did not exert estrogenic activity in vivo at the tested doses. Data suggest that fenvalerate treatment in this study failed to compromise fertility, possibly due to enhanced reproductive capacity in rodents compared to humans.

The aim of this study was to investigate long-term effects of prenatal betamethasone exposure on sexual partner preference, testosterone level, and sexual behavior. Pregnant rats received 0.1 mg/kg of betamethasone or saline on the 12th, 13th, 18th, and 19th days of pregnancy. Parameters in male offspring were evaluated at 90 days of age. Male rats from the betamethasone group did not show any difference in sexual partner preference as expressed by the total number of visits to the female or male zone. However, these males spent significantly less total time and shorter duration per visit in the female zone than their controls. Therefore, prenatal exposure to betamethasone led to a significantly lower sexual female partner preference score compared to the control group. These animals also presented diminished testosterone levels in adulthood. Prenatal exposure to betamethasone induced a delay in the latency to first ejaculation, as well as a decrease in the numbers of postejaculatory intromissions, total intromissions and total ejaculations. Although 80% of the betamethasone-treated animals exhibited male sexual behavior, when they were castrated and pretreated with estrogen, 50% of them showed lordosis and accepted mounts of another sexually experienced male. These results suggest that the prenatal treatment with betamethasone, by increasing maternal corticosteroid level, may have diminished testosterone peak in male pups, a peak crucial to brain sexual differentiation. As a consequence, the prenatal betamethasone treatment reduced the testosterone level in adulthood and altered partner preference and sexual behavior.