Neonatal exposure to diethylstilbestrol leads to impaired action of androgens in adult male hamsters.

Neonatal treatment with diethylstilbestrol (DES) leads to disruption of spermatogenesis in adult animals after apparently normal testicular development during puberty indicating aberrant androgen action in DES-exposed adult hamsters. The present study determined the effects of exogenous androgens in neonatally DES-exposed hamsters. Exogenous androgens failed to reverse the disruption of spermatogenesis in DES-exposed animals. Neonatal DES exposure caused a significant decrease in seminal vesicle weight, and abnormal histology. While exogenous androgens caused a significant increase in seminal vesicle weight in control animals, they failed to restore the seminal vesicle weight and normal histology in DES-exposed animals. Northern blot and/or RT-PCR analysis revealed that (1) AR, ERalpha and ERbeta mRNA levels were unchanged in DES-exposed animals, and (2) mRNA levels for the AR-responsive genes calreticulin, SEC-23B, and ornithine decarboxylase were significantly decreased in DES-exposed animals. Our results suggest that neonatal DES exposure impairs the action of androgens on target organs in male hamsters.