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PERIPUBERTAL DEHP EXPOSURE INHIBITS ANDROGEN-DEPENDENT DEVELOPMENT IN SPRAGUE-DAWLEY RATS
Citation:
Noriega, N C., J. R. FURR, C. R. LAMBRIGHT, V. S. WILSON, AND L. E. GRAY, JR. PERIPUBERTAL DEHP EXPOSURE INHIBITS ANDROGEN-DEPENDENT DEVELOPMENT IN SPRAGUE-DAWLEY RATS. Presented at Society of Toxicology, New Orleans, LA, March 6-10, 2005.
Description:
Peripubertal DEHP exposure inhibits androgen-dependent development in Sprague-Dawley rats.
N.C. Noriega, J. Furr, C. Lambright, V.S. Wilson and L.E. Gray.
noriega.nigel@epa.gov
US EPA, MD-72 RTD, NHEERL, ORD, RTP, NC 27711
The plasticizer Di (2-ethylhexyl) phthalate (DEHP) may present reproductive risk by demasculinizing prenatal and juvenile males. The current study was designed to assess DEHP effects throughout pubertal development in Sprague-Dawley rats. Males were dosed with DEHP at 0, 100, 300 and 900 mg/kg-bw/day from PND 23. A |*dprime*|peri-pubertal|*dprime*| group was dosed until mid puberty (euthanized on PND 43/44), and a |*dprime*|post-pubertal|*dprime*| group was dosed throughout puberty (euthanized on PND 63/64). At the time of first necropsy, where half of the male study population was euthanized, there was a dose dependent reduction in the number of males showing complete preputial separation. Females dosed daily from PND 23 with either corn oil or 900 mg/kg-bw/day DEHP showed no differences in time to vaginal opening. In males, weights of androgen dependent tissues (testis, epididymis, ventral prostate, seminal vesicle, Cowper|*prime*|s glands and levator ani + bulbocavernosus muscles were reduced at high doses in peri and post-pubertal groups. Serum testosterone (T) levels and adrenal gland weights showed dose dependent reductions in the peri-pubertal group, but were not significantly affected in the post-pubertal group. |*bital*|Ex-vivo|*eital*| testis T production was reduced (with and without gonadotropin stimulation) in a dose-dependent manner in peri and post-pubertal groups. On a per weight basis (T/mg of testis), there was a dose dependent increase in |*bital*|ex-vivo|*eital*| testis T production in the post-pubertal group. These findings support the hypothesis that DEHP treatment around early puberty decreases Leydig cell T output, whereas prolonged treatment throughout puberty increases Leydig cell T output. These data do not support the hypothesis that DEHP exposure promotes precocial pubertal development by elevating serum T. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.