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BOR - Papers in Press, published online ahead of print October 17, 2002.
Biol Reprod 2002, 10.1095/biolreprod.102.008078
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BIOLOGY OF REPRODUCTION 68, 465–471 (2003)
DOI: 10.1095/biolreprod.102.008078
© 2003 by the Society for the Study of Reproduction, Inc.

Mechanisms of Hormone Action

Chronic Administration of Anabolic Steroids Disrupts Pubertal Onset and Estrous Cyclicity in Rats1

Ann S. Clark2,a, Megan C. Keltona, and Andrew C. Whitneya

a Department of Psychological and Brain Sciences, Dartmouth College, Hanover, New Hampshire 03755

Use of anabolic-androgenic steroids (AASs) is becoming increasingly popular among adolescent girls, yet the effects of AASs on female physiology and development are not well understood. The present study compared the effects of chronic exposure to three individual AASs, stanozolol (0.05–5 mg/kg), 17{alpha}-methyltestosterone (0.5–5 mg/kg), and methandrostenolone (0.5–5 mg/kg) on the onset of puberty and estrous cyclicity in the rat. Female rats received daily injections of AASs for 30 days (Postnatal Day [PN] 21–51). Rats receiving the highest dose of each of the AASs (5 mg/kg) displayed vaginal opening at a younger age than rats receiving the oil vehicle. The day of first vaginal estrus was delayed in rats receiving stanozolol (5 mg/kg) or 17{alpha}-methyltestosterone (0.5–5 mg/kg) but not in rats receiving methandrostenolone. At the highest dose (5 mg/kg), each of the AASs reduced the incidence of regular estrous cyclicity during the treatment period. Concurrent administration (on PN21–51) of the androgen receptor antagonist, flutamide (10 mg/kg, twice daily), reversed the effects of 17{alpha}-methyltestosterone (5 mg/kg) on vaginal opening. Flutamide administration also eliminated the effects of stanozolol (5 mg/kg) and 17{alpha}-methyltestosterone (5 mg/kg) on the day of first vaginal estrus. In contrast, rats receiving flutamide and methandrostenolone (5 mg/kg) exhibited first vaginal estrus earlier than controls. The present results indicate that chronic exposure to AASs during development has deleterious effects on the female neuroendocrine axis and that these effects appear be mediated via multiple mechanisms.

1 This work was supported by NIH grant DA08574 to A.S.C.

2 Correspondence: Ann S. Clark, Department of Psychological and Brain Sciences, Dartmouth College, 6207 Moore Hall, Hanover, NH 03755. FAX: 603 646 1419; ann.s.clark{at}dartmouth.edu






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Copyright © 2003 by the Society for the Study of Reproduction.