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DEVELOPMENTAL EXPOSURE TO AN ENVIRONMENTAL ANDROGEN, 17 B TRENBOLONE, CAUSES REPRODUCTIVE MALFORMATIONS AND REDUCED REPRODUCTIVE OUTPUT IN FEMALE RATS
Citation:
HOTCHKISS, A. K., J. R. FURR, AND L. EARL GRAY. DEVELOPMENTAL EXPOSURE TO AN ENVIRONMENTAL ANDROGEN, 17 B TRENBOLONE, CAUSES REPRODUCTIVE MALFORMATIONS AND REDUCED REPRODUCTIVE OUTPUT IN FEMALE RATS. Presented at Triangle Consortium for Reproductive Biology, Chapel Hill, NC, January 27, 2007.
Description:
Recently, studies have detected environmental androgen-active chemicals in effluents from pulp mills and animal feedlot operations. One such chemical present in feedlot discharge is the growth promoter, trenbolone acetate. A primary metabolite of trenbolone acetate, 17ß trenbolone (TB), is a potent androgen in both in vitro and in vivo studies. However, TB, similar to other C-19 norandrogens, displays tissue-selective androgenic effects in castrate male rats due to the potential inability of TB to be locally reduced to the more potent androgen, dihydrotestosterone (DHT). In this poster, we present the results of a study characterizing the permanent reproductive/developmental effects of prenatal trenbolone exposure on female rats. Further, we compare the potency of developmental exposure to TB to testosterone propionate (TP) for a number of different reproductive endpoints. Female offspring exposed to 0.5, 1.0, or 2.0 mg/d TB on gestational days 14-19 displayed increased anogenital distance at postnatal day 2 (PND 2) and decreased numbers of normal areolae/nipples at PND 13 and as adults. Females exposed to TB in utero, displayed delayed puberty and decreased reproductive output. Further, TB-treated females displayed increased incidences of external genital malformations (e.g. cleft phallus, vaginal opening absent) and the presence of prostatic tissue, not normally found in females of this species. Interestingly, malformations were displayed in adult females exposed prenatally to either TB or TP, suggesting that TB is capable of significantly affecting testosterone-dependent tissues, as well as DHT-dependent tissues.