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(P723) Increased kidney and testicular cell death after developmental exposure to 17-ethinylestradiol in medaka (Oryzias latipes).
Weber, Lynn*,1, Balch, Gordon2, Metcalfe, Chris2, Janz, David1, 1 Oklahoma State University, Stillwater, OK, USA2 Trent University, Peterborough, ON
ABSTRACT- Sublethal effects (e.g. reproductive toxicity) observed in fish exposed to environmental estrogens may be mediated via stimulation of cell death. To investigate whether apoptosis or necrosis is induced in fish after developmental exposure to estrogenic chemicals, Japanese medaka (Oryzias latipes) were exposed from 1 day post-hatch until sexual maturity to 10 ng/l 17-ethinylestradiol (EE) or acetone solvent (control). Cell death was evaluated in blinded histological sections of whole medaka using Tdt-mediated dUTP nick end-labeling (TUNEL) which labels nuclei of cells containing apoptotic or necrotic (fragmented) DNA. The major impact of EE exposure in both male and female medaka was to significantly increase the number of TUNEL-positive kidney tubule cells compared to control (n=9-24 fish per group and sex) and morphology was consistent with cloudy swelling or necrosis. The number of TUNEL-positive interstitial (hematopoietic) and glomerular cells was significantly greater in EE-exposed male, but not female medaka kidney. However, glomerular dilation and increased intercapsular space was observed in both sexes in EE compared to control fish. EE exposure also significantly increased the number of TUNEL-positive medaka testicular cells compared to corresponding controls, primarily in dense aggregates at the edge of spermatocysts. These cells were identified as Sertoli cells, spermatocytes and spermatids. In medaka with ovatestes, areas of fibrosis or those near female gonadal cells were relatively unstained with TUNEL. There was no effect of EE exposure on the number of TUNEL-positive ovarian somatic cells or on the rate of female ovarian follicle atresia. Finally, EE exposure had no effect on TUNEL in liver, gill or intestine in medaka. These results suggest that developmental exposure to EE in medaka is nephrotoxic in both sexes, but is more severe in males. Furthermore, developmental exposure to EE increases cell death in testicular, but not ovarian cells in medaka.
Key words: 17-ethinylestradiol, apoptosis, testes, kidney
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