Consumption of Xenoestrogen-Contaminated Fish during Lactation Alters Adult Male Reproductive Function

Abstract

Little information exists on the transfer of endocrine-disrupting effects through the food chain. The transfer of chemicals, particularly from the aquatic ecosystem, that can cause such effects on fish-eating predators must be established. Fish from the St. Lawrence River are exposed to xenoestrogens causing male reproductive dysfunction. The objective of this study was to determine if lactational exposure to contaminated fish could alter the development of the male reproductive system in rats. Three experimental groups were used: rats (dams) gavaged with (a) distilled water (control), or (b) homogenized fish from a reference site (Iles de la Paix) or (c) homogenized fish from a xenoestrogen-contaminated site (Ilet Vert). Pups were exposed via lactation and sampled on either day 21 (weaning) or day 91 (adults). There was no effect on the body weights or in the male reproductive organ weights between groups except for adult epididymal weight, which was significantly decreased in the xenoestrogen group. Adult sperm concentrations and sperm motility parameters were all significantly decreased in the xeonestrogen group as compared to the reference and control groups. Furthermore, the distribution of stages of spermatogenesis was altered in the xenoestrogen group, indicating an effect on the kinetics of spermatogenesis. Immunoreactivity of connexin43 (Cx43), a gap-junctional protein, was markedly decreased in the seminiferous epithelium of the xenoestrogen group, suggesting that the intercellular coordination of testicular function may be affected. These data indicate that contaminants from xenoestrogen environments may pass through the food chain and exert effects on male reproductive functions.

Aneuploid sperm formation in rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

“…Through these actions environmental estrogens affect vertebrate reproduction across a wide range of doses causing reduced fertility and fecundity, altered reproductive behavior, gonad morphological changes, and decreased embryonic survival (25)(26)(27)(28)(29)(30)(31)(32)(33)(34). Although both sexes are affected, males exhibit the highest degree and number of detrimental effects.…”

“…Although both sexes are affected, males exhibit the highest degree and number of detrimental effects. Specific male defects caused by environmental estrogen exposures in vertebrates include: intersex (25,29), diminished sperm count (27,(35)(36)(37), genital tract alterations (38), increased germ cell apoptosis (30,33), and male induced embryonic mortality (31,39).…”

“…Although most rodent model studies show decreased sperm production and/or increased apoptosis of germ cells after exposure (27,30,33,35), others have failed to confirm these findings (40). Additionally, recent in vitro exposures of human spermatozoa to catechol estrogens (e.g., quercetin, diethylstilbestrol and pyrocatechol) indicate an impact on sperm DNA integrity through altered redox cycling, but estrogen (17␤-estradiol) and other estrogen analogues (nonylphenol and BPA) do not show this effect (41).…”

Effects of a major municipal effluent on the St. Lawrence River: A case study

“…4b). Histological analyses of the testes of these fish indicate that almost 35 % of fish captured near sewage outfall exhibit intersex (Aravindakshan et al 2004a). Spermatogenesis requires coordinated intercellular communication, as mediated by gap junctions shown to be essential for spermatogenesis in the mammalian testis.…”

“…In a more extensive study, spottail shiners were shown to be exposed to environmental estrogens in the SLR. This contamination begins approximately 20 km upstream from the Island of Montreal, and although it results from several inputs including the Ottawa River, sewage effluents from Montreal contribute the greatest charge in estrogenic compounds (Sabik et al 2004;Aravindakshan et al 2004a). Male spottail shiners captured near the WWTP discharge point exhibit elevated levels of VTG and altered reproductive functions, including delayed spermatogenesis, decreased sperm counts, altered sperm motility, and a significantly greater concentration of static sperm (Fig.…”