The 17-oxidation of testosterone was studied in 6 normal men (age 18–35) and 4 normal menstruating women (age 18–45) by administering iv tracers of 17α-3H-4-14C-testosterone and determining the rate and extent of appearance of 3H in body water. No significant sex difference was found, either in the kinetics or extent of oxidation. At 24 hr, by which time oxidation was complete, the body water contained an average of 61% of the administered 3H(range 43–76) in men; in women the average was 67% (range 59–70). The absence of a sex difference in 17-oxidation of testosterone contrasts sharply with the previously reported striking sex difference in 17-oxidation of estradiol (1). The extent of 17-oxidation exceeded by about 10% of the dose the reported normal recovery of etiocholanolone plus androsterone after 14C-testosterone tracers. This difference probably represents the extent of formation of further hydroxylated 17-ketonic metabolites of testosterone, e.g., 18-hydroxyandrosterone and 7β-hydroxy-etiocholanolone. The 3H/14C ratio of testosterone isolated from urine was consistently about 20% higher than that of the injected tracer. This was attributed to a primary isotope effect of 3H on the 17-oxidation reaction, leading to 3H enrichment of the unoxidized testosterone. The 3H/14C ratio of etiocholanediol isolated from urine was essentially identical to that of the testosterone in each of the 4 subjects in whom comparison was made. This confirms the existence of the “17β-hydroxy pathway” of formation of etiocholanediol from testosterone, and indicates that any alternate pathway that includes a 17-ketonic intermediate (e.g., testosterone → Δ4-androstenedione → etiocholanolone → etiocholanediol) must be nonexistent or of negligible magnitude.
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Zumoff et al. (1973) studied this question.