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Goyal, H.O. et al.

Goyal, Braden, Williams, Dalvi, Williams, Srivastava,

Exposure of neonatal male rats to estrogen induces abnormal morphology of the penis and loss of fertility.

The research objectives are to determine whether estrogen-induced infertility is associated with abnormal morphology of the penis and if morphological alterations can be reversed by testosterone ( T). Male pups received diethylstilbestrol (DES) on alternate days from postnatal days 2 to 12. They received T or empty implants at 180 days, were tested for fertility at 188 days, and terminated at 200 days. While 5/7 control males sired pups, only 1/6 did in the DES group, and 0/8 in the DES plus T group. In addition to reductions in penile length and weight, the novel structural change induced by DES, and not reversed by T, was a replacement of cavernous spaces by fat cells in the penis body. Hence, T substitution for 8 days at adulthood did not reverse infertility in rats treated neonatally with DES and provided evidence that infertility probably resulted from absence of cavernous spaces and/or accumulation of fat cells in the penis body.[1]

References

Exposure of neonatal male rats to estrogen induces abnormal morphology of the penis and loss of fertility. Goyal, H.O., Braden, T.D., Williams, C.S., Dalvi, P., Williams, J.W., Srivastava, K.K. Reprod. Toxicol. (2004) [Pubmed]

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