Fish pollutants MeHg and Aroclor cause permanent structural damage in male gonads and kidneys after prepubertal exposure

Abstract

This study investigated whether or not prepubertal exposure to the fish contaminants methylmercury (MeHg) and the polychlorinated bisphenol Aroclor in low doses interferes with the histomorphometry of the testes, epididymis, liver and kidneys in rats. Wistar male rats, 21 days old, were allocated into the following: control (n = 17, received corn oil), MeHg (n = 17, received MeHg at 0.5 mg/kg/day), Aroclor (n = 17, received Aroclor at 1.0 mg/kg/day), low mix (n = 18, received MeHg at 0.05 mg/kg/day and Aroclor at 0.1 mg/kg/day), high mix (n = 18, received MeHg at 0.5 mg/kg/day and Aroclor at 1.0 mg/kg/day). Dosing continued from post natal day (PND) 23 to 53, by gavage. Euthanasia was performed on PND 53; or, after an interval of 62 days without exposure to chemicals, on PND 115. The degree of maturation of the seminiferous epithelium was delayed in chemical-exposed groups and testicular interstitial oedema was observed at adulthood. The pattern of male gonad organization was changed in the Aroclor group on PND 53 and in all treated groups at adulthood. The animals from Aroclor, low mix and high mix groups showed a reduction in the number of Sertoli cells. Histological evidence of renal injury was observed in all chemical-exposed groups in both ages. A probable target for MeHg and Aroclor in the reproductive system was Sertoli cells, in which possible dysfunctions could be linked to the other testicular alterations. Curiously, the main deleterious effects were late outcomes, along with the absence of synergistic interaction of MeHg and Aroclor in the parameters investigated. In conclusion, fish pollutants MeHg and Aroclor caused permanent structural damage in male gonads and kidneys after prepubertal exposure, without showing clear chemical interactions.

Molecular Mechanisms and Signaling Pathways Involved in Sertoli Cell Proliferation

“…Nowadays, it is well-known that testis function is a primary target of a large number of pollutants. Delayed establishment of spermatogenesis (295), impaired differentiation of internal and external male genital structures (296), reduced sperm production and disruption of the hypothalamic–pituitary–gonadal axis (297), decreased anogenital distance and decreased prostate and seminal vesicle weights (298, 299), among others, represent just some of the multiple observations performed.…”

In vivo evaluation of the potential protective effects of prolactin against damage caused by methylmercury

“…Histopathological analysis demonstrated varied changes in renal and hepatic tissue in all treatments, although this damage was generally most frequent and intense in the animals of the MeHg group. Renal alterations promoted by MeHg, such as hypertrophied glomeruli and tubular lesions, had already been demonstrated in small rodents by Garcia et al ( 23 ) and Khan et al ( 24 ), respectively. Damage caused by mercury compounds, such as those found in the present study, was also identified in the liver of these mammals, ( 25 , 26 ).…”

Zooplankton Feeding Induces Macroscopical Gonad Malformations in Whitefish (Coregonus ssp.) from Lake Thun, Switzerland

“…Accordingly, gonad abnormalities of fish have been associated, among others, with genetic quality and hybridization status of the broodstock [18,19], autoimmune disease [20], changes in physical water parameters [21,22] or parasite infection [23,24]. One environmental factor that has attracted particular attention as a cause of gonad abnormalities in fish is aquatic contamination by anthropogenic chemicals [4,15,[25][26][27][28][29][30]. Obviously, a broad variety of factors can be involved in the induction of gonad morphological alterations in fish, and to advance our understanding of this phenomenon, it needs a systematic approach to unravel the causative factors and processes.…”