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Daily hormonal studies during nine ovulatory menstrual cycles showed that plasma prolactin and testosterone concentrations fluctuated randomly and independently. Mean plasma testosterone levels were found to be higher during the 7 days before and after the mid-cycle LH peak when compared to the premenstrual phase (P less than 0-01). No correlation was found between daily levels of prolactin and those of LH, FSH, oestrogen or progesterone and no correlation was seen between peaks of prolactin and testosterone or mean prolactin and testosterone levels. The lack of correlation between blood levels of prolactin and testosterone during the menstrual cycle suggests that prolactin is unlikely to have any direct controlling influence on the cyclical nature of testosterone production observed during ovulatory menstrual cycles.

Current methods for measuring testicular hormonal function are based on the fact that the testis secretes androgen. The results obtained are often of limited value, since the adrenal cortex, as well as the testis, is an important source of androgen. For example, the levels of androgen' and 17-ketosteroids? in the urine of castrated individuals frequently fall within the range for normal men. Obviously, measurement of substances more exclusively testicular in origin might offer a better indication of testicular function. men excrete less than normal amounts of estrogen suggests the testis as a source of estrogen in men, little attention has been given to the possible value of estrogen assays in measuring the hormonal function of the testis. In this study, therefore, both urinary estrogen and 17-ketosteroid determinations were employed in investigating testicular function. For the results to have more than empirical value, the origin and mechanisms controlling production of these substances should be known. It is generally agreed that 17-ketosteroids of testicular origin are metabolites of androgen secreted by Leydig cells, but no such agreement exists as to the source of testicular estrogen. Some investigators have considered the Sertoli cells to be the origin,'' 8 , 9 , lo whereas others have concluded that the Leydig cells are the most likely source.ll' l2In addition to comparing estrogen and 17-ketosteroid determinations as indicators of testicular hormonal function, this study necessarily has been concerned with the questions of origin and mechanisms controlling estrogen production in men. Two methods of studying these questions have been employed. First, estrogen and 17-ketosteroid excretion of normal men was compared with that of men having abnormal testicular function. Second, changes in estrogen and 17-ketosteroid excretion produced by administration of chorionic gonadotrophin and luteotrophin were correlated with alterations occurring in testicular morphology. MethodsUrinary estrogens were determined by the methods previously described.13 I n brief, acidified urine is hydrolyzed by boiling and then extracted with chloroform. The alkali-soluble fraction of the chloroform extract is acidified with hydrochloric acid and extracted with ether. This extract is then dissolved in sesame oil and administered twice daily for three days to immature female Sprague-Dawley rats. Increases in uterine weight produced by the extract Although the observation that castrated" 3 , and eunuchoidaF~ 5 ,

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