4.7 Article

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

Journal

CHEMICO-BIOLOGICAL INTERACTIONS
Volume 333, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2020.109314

Keywords

Sodium arsenite; Oxidative stress; Antioxidant genes; Pre-puberty; Male reproductive development

Funding

  1. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais [PPM-00621-18]
  2. Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro [211.225/2019]
  3. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [150333/2018-8]

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Exposure to arsenic during pregnancy has negative effects on the reproductive development of male rats, leading to reduced body weight, inhibited testicular development, and decreased hormone levels. Additionally, signs of oxidative stress were observed in the prepubertal male rats exposed to arsenic.
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.

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