title: 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.
authors.affiliation: INRS-Institut Armand Frappier, Université du Québec, Montreal, Quebec, Canada H9R 1G6.
authors.forename: Jayaprakash
authors.initials: J
authors.lastname: Aravindakshan
authors.forename: Mary
authors.initials: M
authors.lastname: Gregory
authors.forename: David J
authors.initials: DJ
authors.lastname: Marcogliese
authors.forename: Michel
authors.initials: M
authors.lastname: Fournier
authors.forename: Daniel G
authors.initials: DG
authors.lastname: Cyr
mesh_terms: D000818:Animals; D000833:Animals, Suckling; D001835:Body Weight / Q000187:drug effects; D018031:Connexin 43 / Q000378:metabolism; D004785:Environmental Pollutants / Q000032:analysis / Q000633:toxicity*; D004822:Epididymis / Q000473:pathology; D004968:Estrogens, Non-Steroidal / Q000032:analysis / Q000633:toxicity*; D005260:Female; D005399:Fishes; D020387:Food Chain; D005506:Food Contamination; D007150:Immunohistochemistry; D007774:Lactation / Q000502:physiology*; D008297:Male; D008460:Meat; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012098:Reproduction / Q000187:drug effects*; D013081:Sperm Motility / Q000187:drug effects; D013091:Spermatogenesis / Q000187:drug effects; D013737:Testis / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000378:metabolism; D014819:Vitellogenins / Q000096:biosynthesis; D015262:Xenobiotics / Q000032:analysis / Q000633:toxicity*
chemical_list: D018031:Connexin 43; D004785:Environmental Pollutants; D004968:Estrogens, Non-Steroidal; D012333:RNA, Messenger; D014819:Vitellogenins; D015262:Xenobiotics; D013739:Testosterone