title: Effect of 17beta-estradiol, o,p'-DDT, octylphenol and p,p'-DDE on gonadal development and liver and kidney pathology in juvenile male summer flounder (Paralichthys dentatus).
abstract: The intent of this study was to compare histopathologically the effect of 17beta-estradiol (E(2)), o,p'-DDT, octylphenol and p,p'-DDE on gonadal development and liver and kidney condition in sexually immature (juvenile) summer flounder (Paralichthys dentatus). The dorsal sinus of 2-year-old juvenile male summer flounder was injected with the appropriate amount of chemical incorporated in coconut oil. A second identical injection was administered 2 weeks later. Fish were sampled at 4, 6 and 8 weeks after the initial injection and observed histopathologically. In control fish, spermatogenesis was predominantly in mid to late maturation. In fish treated with 1.0 and 10.0 mg/kg E(2) spermatogenesis regressed to primary spermatogonia or an immature functional state. Testicular atrophy and spermatogonial proliferation was also observed. An eosin-positive, hyaline material was found in the gonad, liver and kidney. This eosinophilic material also stained positive with Periodic Acid Schiff (PAS) stain. Treatment of 30 or 60 mg/kg o,p'-DDT elicited altered gonadal development similar to that observed with E(2) treated fish. Octylphenol treatment of 100 mg/kg resulted in reduced testicular size, ducts full of sperm, numerous spermatogonia and PAS positive material in the testis with no developing sperm cysts. No effect on liver or gonad tissues was observed with p,p'-DDE at the concentrations tested. All chemicals tested, with exception of p,p'-DDE, altered gonadal development, whereas only E(2) caused histopathological changes in the liver and kidney. Estrogenic activity induced the liver to produce a vitellogenin (VtG)-like substance and inhibited testicular maturation. As a result, both the lack of target cells for VtG and a continuous supply of VtG from the liver allowed the hyaline material to accumulate in the liver, testis and kidney causing histopathological changes.
authors.affiliation: US Environmental Protection Agency, NHEERL/AED, 27 Tarzwell Drive, Narragansett, RI 02882-1154, USA. Zaroogian.Jerry@epa.gov
authors.forename: G
authors.initials: G
authors.lastname: Zaroogian
authors.forename: G
authors.initials: G
authors.lastname: Gardner
authors.forename: D B
authors.initials: DB
authors.lastname: Horowitz
authors.forename: R
authors.initials: R
authors.lastname: Gutjahr-Gobell
authors.forename: R
authors.initials: R
authors.lastname: Haebler
authors.forename: L
authors.initials: L
authors.lastname: Mills
mesh_terms: D000818:Animals; D003634:DDT / Q000633:toxicity*; D003633:Dichlorodiphenyl Dichloroethylene / Q000633:toxicity*; D004958:Estradiol / Q000633:toxicity*; D005260:Female; D005432:Flounder; D006066:Gonads / Q000187:drug effects* / Q000254:growth & development / Q000473:pathology; D007668:Kidney / Q000187:drug effects* / Q000473:pathology; D008099:Liver / Q000187:drug effects* / Q000473:pathology; D008297:Male; D010636:Phenols / Q000633:toxicity*; D013737:Testis / Q000187:drug effects / Q000473:pathology
chemical_list: D010636:Phenols; D003633:Dichlorodiphenyl Dichloroethylene; D004958:Estradiol; C080417:4-octylphenol; D003634:DDT; C016340:o,p'-DDT