Abstract

Male mice were injected either with cyproterone acetate (CyAc) or with testosterone enanthate (TE) separately or in combination with estradiol benzoate (E2B) from the neonatal period on or during adulthood. Neonatally treated animals were killed on d28 or d60, whereas all treated adults were killed on d60. Synaptonemal complexes (SCs) were analyzed under the electron microscope. Various SC anomalies were recorded. The frequency of SC alterations was higher in neonatally treated mice injected with E2B alone or in combination with CyAc (range 9.6–23.7%) than in those injected separately with TE or CyAc (range 2–3.9%). In treated neonates, combination of CyAc and E2B treatment increased the prevalence of synaptic impairments (range 11–23.5%). However, whenever TE was added to E2B treatment a significant reduction of these impairments was observed (range 11–2.4 and 23.7–9.7% respectively). In treated adult mice the prevalence of SC anomalies was low (range 2.4–3.1%) whatever hormone was injected. Furthermore, the combination of estradiol with CyAc had no increasing effect on the induction of synaptic alterations. In E2B-treated animals, those injected during the neonatal period were more susceptible than those treated in adulthood. In mice injected separately with TE or CyAc such a difference of sensitivity between neonates and adults was not noticeable. This work demonstrates that testosterone deficiency is partly responsible for E2B-induced SC alterations. However, inhibition of testosterone action at the level of testicular target cells, such as that resulting from administration of cyproterone acetate, is less harmful to the synaptic process of meiosis.

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