An endocrine mechanism involved in testicular changes produced by a dl-ethionine supplemented diet: a study of morphologic changes and endocrine dysfunction.

Abstract

The endocrine-morphological relationship in testicular lesions of rats treated with ethionine and testosterone was investigated. This was done through indirect evaluation of the androgenic activity by the estimation of urinary 17-KS excretion. It has been found that small and large doses of testosterone (12 clays of treatment) prevent histologic testicular changes clue to ethionine. However small doses of testosterone given over a longer period (24 days) did not prevent ethionine-induced testicular histologic changes. Large doses of testosterone did not prevent damage to spermatogenesis during continuous ethionine administration, but did prevent Leydig cell hyperplasia. Ethionine alone stopped spermatogenesis, and induced Leydig cell hyperplasia. Leydig cell hyperplasia therefore may have been compensatory. Ethionine treatment decreased the excretion of 17-KS prior to the appearance of any testicular morphological changes. Therefore ethionine presumably affected the androgenic activity directly if 17-KS excretion may be used as an index of androgenic activity. Intraperitoneal (I.P.) administration of ethionine diminished the 17-KS excretion by two thirds. Since I.P. ethionine diminished in 12 days the excretion of 17-KS in the absence of histologic testicular changes and was followed by an increase in the excretion of 17-KS associated with Leydig cell hyperplasia after 24 days, this would suggest that functional changes precede histologic changes. Morphological liver changes were demonstrable within 24 days after initiating oral ethionine therapy but not after I.P. ethionine. Gastrointestinal versus systemic absorption of the administered ethionine may be a factor. Finally, it may be concluded that an endocrine-morphological relationship exists in the pathogenetic effect of ethionine on testicular changes observed in albino rats.