Abstract
Within 48 h of EDS [ethane 1,2-dimethane sulfonate] [nonsteroidal antifertility agent] injection in vivo the capacity of testicular tissue to release c [cyclic] AMP when stimulated by HCG [human chorionic gonadotropin] was almost abolished. The trend was also apparent at 4 h after EDS treatment. The fall in HCG response occurs much earlier than the decline in steroidogenesis following a similar dose of EDS; testosterone formation has fallen to only half its normal rate by 60 h after EDS injection. EDS interferes with the ability of testicular tissue to respond to LH [luteinizing hormone], normally one of the most important stimulators of the testis, because of the failure to produce the cAMP mediator.

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