Gegenwärtiger Stand der Fertilitätshemmung beim Mann

Monensin was given orally to female rats at two dose levels (1.75 and 3.50 mg/kg body weight) over the period of 9-17 days of pregnancy where organogenesis of fetuses occur. The dams were killed on the nineteenth day of gestation and their fetuses were subjected to morphological, visceral and skeletal examination. The small dose of monensin increased the number of resorbed and dead fetuses and induced marked retardation in growth of viable fetuses, but visceral or skeletal defects in these fetuses were not seen. Large doses produced fetal resorption in all dams and no viable fetuses were delivered. Prolonged oral administration of monensin in male rats for 60 successive days at two dose levels, decreased the conception rate in non-treated females (mated with treated males) to 33.3% and 0% for the small and large doses, respectively. Both doses markedly decreased the weights of testicles, epididymides and seminal vesicles. The small dose of monensin caused oligospermia, whereas the large dose induced azospermia. Both doses decreased the activity of spermatogenic epithelium and caused degeneration in germ cells after histopathological examination of the testicles. It is concluded that monensin given during pregnancy to female rats is fetotoxic and when administered chronically to male rats, causes damage to the reproductive organs. The delayed effects of this drug are especially prominent.

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