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THE mechanism by which the liver inactivates2 various steroid hormones has been the subject of numerous investigations since Zondek (1934) first demonstrated the inactivation of estrogen by this organ. Interest in the metabolism of estrogens seems to have been more extensive than interest in the metabolism of androgens. Six years after Zondek’s observation with estrogens, Biskind and Mark (1939) demonstrated that pellets of testosterone propionate implanted in the spleen did not effect weight changes in the prostate or seminal vesicles of castrate rats. They observed that pellets implanted subcutaneously, or into a subcutaneously transplanted spleen, caused a marked increase in the size of the male accessories. From this evidence, they suggested that the liver was the site of inactivation of testosterone propionate. Later, these observations were extended to methyl testosterone and testosterone (Burrill and Greene, 1942). The former caused slight prostatic enlargement when implanted in the spleen.
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Grayhack et al. (1951) studied this question.
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