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The present studies are related to the effects of oral administration of lead acetate on rat spermatogenesis. In addition to the observations of greatly inhibited sperm motility and a reduced sperm count in the lead acetate-fed rats, as obtained in our earlier studies [Leblond et al.: Physiol Rev 52:198–236, 1972], it was considered important to study the cell kinetics in the seminiferous epithelium, a site for the generation of sperm. Lead-induced shrinkage of the seminiferous tubules was observed with a significant decrease in tubular diameter and germinal height. An overall decrease in all cell types was seen with maximum lead acetate effects on the fully mature spermatids. A ratio between the number of cells at various sequential stages was also determined. The ratios of the young spermatids to the pachytene spermatocytes and the mature spermatids to young spermatids were significantly low in the different lead-treated groups. Some depression of spermatogenesis at the young spermatid stage was observed at higher lead acetate doses. However, the arrest of spermatid maturation at the lowest dose of lead was complete. The maximum toxicity at the lowest dose of lead probably relates to the bioavailability of lead, which may be checked by the induction of lead-binding proteins as the higher lead levels.
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Kaushal et al. (1996) studied this question.
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