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GESTATIONAL EXPOSURE TO ETHANE DIMETHANESULFONATE (EDS) ALTERS DEVELOPMENT OF THE MOUSE TESTIS
Citation:
Tarka, D. K., J D. Suarez, N L. Roberts, J M. Rogers, M. P. Hardy, AND G R. Klinefelter. GESTATIONAL EXPOSURE TO ETHANE DIMETHANESULFONATE (EDS) ALTERS DEVELOPMENT OF THE MOUSE TESTIS. Presented at American Society of Andrology, Seattle, Washington, April 24-27, 2002.
Description:
GESTATIONAL EXPOSURE TO ETHANE DIMETHANESULFONATE (EDS) ALTERS DEVELOPMENT OF THE MOUSE TESTIS. D.K. Tarka*1,2, J.D. Suarez*2, N.L. Roberts*2, J.M. Rogers*1,2, M.P. Hardy3, and G.R. Klinefelter1,2. 1University of North Carolina, Curriculum in Toxicology, Chapel Hill, NC; 2USEPA, NHEERL, RTD, RTP, NC, and 3Population Council, NY, NY.
Previously we found that administration of the well known Leydig cell (LC) toxicant, EDS, to pregnant dams (160 mg/kg, i.p.) during gestation days (GD) 11-17 compromised reproductive development in male progeny. On GD 16, EDS toxicity manifested as a diminished testosterone (T) peak, and on GD 18, males had reduced anogenital distance. We sought to determine whether this exposure results in persistent effects throughout reproductive development. Although puberty was delayed as evidenced by delayed preputial separation, hCG-stimulated T production by testis parenchyma was unchanged. However, light micrographs of prepubertal testes from EDS exposed males revealed seminiferous tubule (ST) cross sections containing only Sertoli cells, indicating a delay in the onset of spermatogenesis. As adults, EDS-exposed males had reduced epididymal sperm reserves, and females mated to these males had reduced fertility ratios and litter sizes. Serum LH levels increased as did hCG-stimulated T production per gram of testis. Additionally, the STs were observed to have incomplete germ cell associations. Morphometric analysis revealed an EDS-related increase in interstitial area (934 ? 357 vs. 3184 ? 793 m2) and a concomitant decrease in ST area (21952 ? 3700 vs. 14181 ? 1306 m2), suggesting a relative increase in LCs. Clearly, gestational exposure to EDS can produce profound delays in puberty and spermatogenesis. Thus, while adult mouse LCs are known to be insensitive to EDS, EDS may have direct action on the fetal LC, resulting in abnormal development of the adult testis. (This abstract does not necessarily reflect EPA policy.) DKT: T901915