Impact of prenatal arsenic exposure on the testes and epididymides of prepubertal rats.

Arsenic is a pollutant widely found in the environment due to natural and anthropogenic sources. Exposure to arsenic forms in drinking water has been related with male reproductive dysfunctions in humans and experimental animals at adult age. However, the impact of this pollutant on postnatal reproductive development of male offspring exposed in utero to arsenic is still unknown. Therefore, this study aimed to investigate the effects of prenatal arsenic exposure on the postnatal development of the testes and epididymides of rats, during prepuberty. For this purpose, pregnant female Wistar rats were provided drinking water containing 0 or 10 mg/L sodium arsenite (AsNaO2) from gestational day 1 (GD 1) until GD 21 and the male offspring was evaluated in different periods of prepuberty. Our results showed that prenatal arsenic exposure affected the initial sexual development of male pups, reducing their body weight and relative anogenital distance at postnatal day 1. At different periods of prepuberty, male pups from arsenic exposed dams showed a reduction of body and reproductive organs weights, testosterone levels and testis morphometric parameters. Moreover, these pups presented changes in the expression of SOD1, SOD2, CAT and GSTK1 genes and in the activity of superoxide dismutase, catalase and glutathione s-transferase in the testes and epididymides during prepuberty. Taken together, our results show that prenatal arsenic exposure provoked reproductive disorders in prepubertal male rats, probably due to reproductive reprograming and oxidative stress induced by this pollutant.

Prepubertal exposure to arsenic alters male reproductive parameters in pubertal and adult rats.

Arsenic induces reproductive disorders in pubertal males after prepubertal exposure. However, it is unclear the extent to which those effects remain in testis and epididymis of sexually mature rats after arsenic insult. This study evaluated the effects of prepubertal arsenic exposure in male organs of pubertal rats, and their reversibility in adult rats. Male pups of Wistar rats on postnatal day (PND) 21 were divided into two groups (n = 20/group): Control animals received filtered water and exposed rats received 10 mg L--1 arsenic from PND 21 to PND 51. At PND 52, testis and epididymis of ten animals per group were examined for toxic effects under morphological, functional, and molecular approaches. The other animals were kept alive under free arsenic conditions until PND 82, and further analyzed for the same parameters. Pubertal rats overexpressed mRNA levels of SOD1, SOD2, CAT, GSTK1, and MT1 in their testis and SOD1, CAT, and GSTK1 in their epididymis. In those organs, catalase activity was altered, generating byproducts of oxidative stress. The antioxidant gene expression was unchanged in adult rats in contrast to the altered activity of antioxidant enzymes. Histological alterations of testis and epididymis tissues were observed in pubertal and adult rats. Interestingly, only adult rats exhibited a remarkable decrease in serum testosterone levels. Prepubertal exposure to arsenic caused morphological and functional alterations in male reproductive organs of pubertal rats. In adult rats, these damages disappeared, remained, get worsened, or recovered depending on the parameter analyzed, indicating potential male fertility disorders during adulthood.