Exposure to manganese during sertoli cell formation and proliferation disturbs early testicular development in rats.

Manganese (Mn) is a metal and important micronutrient. However, exposure to supraphysiological levels of Mn, which occur through fungicides, atmospheric emissions, drainages, and spills, has been related to health risks, including morphometric changes in the male reproductive organs and impairment on gametogenesis and sperm quality, impacting the fertile ability of adult animals. Despite the relevance of the fetal/perinatal period for toxicological studies on Mn, previous data only deal with the physical and neurological development of the offspring, without mentioning their reproductive development. The present study investigated whether exposure to Mn during fetal/perinatal phase, specifically during the period of formation and proliferation of Sertoli cells, impairs the reproductive development of male offspring in early postnatal life. Therefore, pregnant Wistar rats were randomly distributed into 3 experimental groups: Ctl (received saline solution), Mn-9 (received 9 mg/kg of MnCl2), and Mn-90 (received 90 mg/kg of MnCl2). The female rats received the experimental treatment by gavage from gestational day 13 to lactational day 15, i.e., postnatal day (PND) 15 of the pups. Oxidative damage to the genetic material of germ and Sertoli cells, together with a decrease in connexin 43 immunolabeling were observed in the testis of male pups evaluated at PND 15. In addition, an increase in the seminiferous tubules presenting slight epithelium vacuolization and cells with eosinophilic cytoplasm were observed, without apparent epididymal changes. In conclusion, it was demonstrated that Mn perturbed the initial testicular development by altering Sertoli cell integrity through oxidative insult, which may compromise the spermatogenesis in the long-term.

Prepubertal exposure to low doses of sodium arsenite impairs spermatogenesis and epididymal histophysiology in rats.

For the first time, juvenile toxicity of inorganic arsenic (As) was investigated in male rats, focusing on reproductive effects. As is a metalloid naturally occurring in the environment, being the inorganic forms the most toxics. Contaminated drinking water and agricultural products are the main prospectors of intoxication for general population. In the present study, Wistar male rats (21 days old) were distributed into three groups (n = 10/group): control (received vehicle-filtered drinking water), As1 (received AsNaO2 at 0.01 mg L-1 ) and As2 (received AsNaO2 at 10 mg L-1 ). The animals were euthanized on PND 53. Testicular damages increased in As1 and As2 compared to control (ie, presence of vacuolization, acidophilic cells, and epithelium degeneration). Testicular interstitium of As1 and As2 presented fluid's increase and intense inflammatory infiltration. In the epididymis there was reduction of sperm amount in the lumen, besides epithelium areas presenting cribriform aspect in As1 and As2, exfoliation of cells in the light (in As1) and vacuoles (in As2). In epididymis interstitium, inflammatory infiltrates were observed in initial segment of As1 and As2. AsNaO2 changed immunolabeling pattern for androgen receptor in epididymis of As2, although serum testosterone levels was statistically comparable to control. Mass spectrometry revealed higher As concentrations in testis and epididymis of As2 compared to As1 and Control. These results indicate compromise of spermatogenesis and epididymal histophysiology in AsNaO2 -treated animals, possibly impairing sperm quality and fertility in long-term, even at low levels of exposure. Investigations about the reversibility of reproductive damages are necessary to better understand the mechanisms of As reproductive toxicity.