Reduced testosterone and Ddx3y expression caused by long-term exposure to arsenic and its effect on spermatogenesis in mice.

Arsenic (As) has been recognized as a cause of male reproductive toxicity. However, effects of long-term arsenic exposure (puberty-adult) on spermatogenesis, testosterone synthesis, and the expression of androgen binding protein (ABP) and Ddx3y remain unclear. The objective of this investigation was to explore these effects and the underlying mechanisms. Male mice were treated with 5 and 50 ppm arsenic for 6 months via drinking water. The results showed that arsenic reduced sperm count and sperm motility and enhanced the abnormal sperm percentage. The decrease in the number of spermatogenic cells and sperm in seminiferous tubules and the decline in the Johnsen score were observed in both arsenic-treated groups, suggesting spermatogenesis disorders. Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-β-hydroxysteroid dehydrogenase (17β-HSD) genes. Arsenic also down-regulated mRNA levels of ABP and Ddx3y in a dose-dependent manner. Meanwhile, the protein levels of StAR, 17β-HSD and Ddx3y were significantly reduced in arsenic-treated groups. Taken together, these results suggest that the reduced testosterone through inhibition of the expression of multiple genes responsible for the biosynthesis, the damaged androgen homeostasis partially via lessening the expression levels of the ABP gene and the down-regulated expression of Ddx3y, may contribute to spermatogenesis disorders in mice exposed to arsenic.

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