A method for estimating catechol estrogen metabolism from excretion of noncatechol estrogens

Abstract

The relationship of catechol estrogen metabolism to disease has seldom been investigated because of analytic difficulties. Estradiol (E2) and estrone (E1) are oxidized simultaneously at either ring A or ring D, and the rate of catechol estrogen formation (r2) is reciprocally related to the rate of 16α‐hydroxylation (r3). The rate of ovarian estrogen production (X10) can be summarized as to metabolic outcome: X10 = r10 + r2 + r3 + ru, where r10 is the loss of E1 and E2 in urine, and ru is the fecal and urinary loss of unknown oxidative products. Assuming a constant ru between subjects: X10 – r10 = r2 + r3. The value r10 is only a very small fraction of X10 and does not affect the constancy of the X10 concentration between subjects during similar menstrual cycle phases. In the absence of xenobiotics, r2 and r3 are reciprocally interrelated: r2 ± r3 = K (an oxidation constant whose limiting factor is the biologically available estrogen at the cell surface). To the extent that r10 approximates estrogens available for cellular metabolism, the rate of catechol estrogen metabolism may be determined fromr2 = (Formula Presented.) From published data K = 12.4 ± 0.8 of the standard error of the mean. Pearson correlation coefficients between actual and estimated catechol estrogen excretion in groups of subjects ranged from 0.61 to 0.97 (median, 0.88). This method has been useful for clinical investigation of the relationship of catechol estrogen metabolism to disease until better methods to measure catechol estrogen directly are available. Copyright © 1991 American Cancer Society