Vitellogenin-induced pathology in male summer flounder ( Paralichthys dentatus)

• Published in: Aquatic toxicology 2001-02, Vol.51 (4), p.431-441
• Main Authors: Folmar, Leroy C, Gardner, George R, Schreibman, Martin P, Magliulo-Cepriano, Lucia, Mills, Lesley J, Zaroogian, Gerald, Gutjahr-Gobell, Ruth, Haebler, Ramona, Horowitz, Doranne B, Denslow, Nancy D
• Format: Article
• Language: English
• Subjects: Agnatha. Pisces; Animal, plant and microbial ecology; Animals; Applied ecology; Biological and medical sciences; Ecotoxicology, biological effects of pollution; Effects of pollution and side effects of pesticides on vertebrates; Estradiol; Estradiol - toxicity; Fish; Flounder - physiology; Fundamental and applied biological sciences. Psychology; Immunohistochemistry; Kidney - pathology; Liver - pathology; Male; Paralichthys dentatus; Pathology; Testis - pathology; Vitellogenin; Vitellogenins - toxicity
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/S0166-445X(00)00121-1

Male summer flounder ( Paralichthys dentatus) were given two injections (initially and 2 weeks later) of 17β-estradiol (E2) totaling 0.2 (2×0.1), 2.0 (2×1.0) or 20.0 (2×10.0) mg E2/kg body weight. Blood and tissue samples were collected 4, 6 and 8 weeks after the initial injection in the (2×0.1) mg/kg treatment, 4, 6, 8, and 15 weeks after the first injection in the (2×1.0) mg/kg treatment and at 4 weeks only in the (2×10.0) mg/kg treatment. Five of the 12 fish injected twice with 10.0 mg/kg were moribund before the first sampling period. Circulating levels of vitellogenin (VTG) in the blood of all E2-injected fish from all treatments were comparable with those concentrations found in the blood of wild male carp ( Cyprinus carpio) and walleye ( Stezostedion vitreum) previously collected near a sewage treatment plant (0.1–10.0 mg VTG/ml plasma). Excessive hyalin material accumulated in the livers, kidneys and testes of the treated fish. A portion of that material was identified as VTG by immunohistochemistry. The accumulation of VTG, and possibly other estrogen-inducible proteins, resulted in hepatocyte hypertrophy, disruption of spermatogenesis, and obstruction or rupture of renal glomeruli.