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PARENT SESSION
2L (1) - Immunotoxicity - genotoxicity - ED Hall 8 1:45 PM - 3:30 PM, Wednesday, 30 April 2003 Chair: Hansen, P.D.1, 1
(WE8/13) Dietary administration of methyltestosterone affects spermatogenesis and male fertility in the Japanese quail.
Niemann, Lars1, Selzsam, Britta2, Fathi, Marion1, Woelffel, Brigitte2, Chahoud, Ibrahim2, 1 Federal Institute of Risk Assessment, Berlin, Germany2 Institute of Clinical Pharmacology and Toxicology, Dept. Toxicology, Berlin, Germany
ABSTRACT- In a one-generation reproduction study, young adult Japanese quail were exposed to the hormone methyltestosterone (MT) at dietary dose levels of 0, 10, 50, and 110 ppm over three weeks. The mean absolute and relative testis weight was decreased at the intermediate dose level by more than 20% and at the highest dose by about 26%. The amount of fertilised eggs was markedly reduced at 50 ppm. At the top dose level, evaluation of the fertilisation rate was not possible since the administration of 110 ppm MT resulted in an immediate and dramatic decrease in the total number of eggs layed. At sacrifice, a dose-related and statistically significant reduction in mean spermatide count was recorded in the groups receiving 50 and 110 ppm. These findings suggest inhibition of spermatogenesis at dose levels of 50 ppm and above resulting in a subsequent reduction in male fertility. Similar effects of MT have been noted in rats. Flow cytometric differentiation of male germ cells according to their DNA content in a limited number of drakes revealed a lower amount of mature ("subhaploid") spermatides and an increase in the diploid cell population in all treated groups but a clear dose-response was lacking. Thus, this sophisticated method provided only rather equivocal evidence of an adverse effect. In contrast to our experience in juvenile Wistar rats, the ratio between somatic and germ cells in the testis was not altered in quail as evidenced by immunostaining of the protein vimentin which is unique to somatic cells.
Key words: Japanese quail, endocrine disrupture, spermatogenesis, male fertility
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