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Abstract
The increase in the testicular blood flow, thought to be a spermatogenesis-accelerating activity of kallikrein, was studied histologically from the viewpoint of how this increase in the testicular blood flow accelerated the testicular damage caused by a high-dose of vinblastine. Damage was evaluated by histological analysis of a germinal cell index and a spermatogenic curve. The results indicated that (a) kallikrein itself did not cause damage to the testis, (b) damage was greater when vinblastine was administered after 10 days' treatment with kallikrein, and (c) the degree of enhancement of the testicular damage was dependent on the amount of kallikrein administered. Damage was first observed in the spermatids, which are highly maturated cells in spermatogenesis and the most dependent on Sertoli cells for their nutrition. Comparison of outer (abound in capillary) and inner regions of the testicular section revealed greater damage in the former. Enhanced testicular damage of both regions was statistically significant in the kallikrein-treated group. Kallikrein increased the peripheral testicular blood flow and accelerated spermatogenesis. Kallikrein may be a useful agent for male fertility.
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