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The Effect of Membrane Permeability and Binding by Human Serum Proteins on Sex Steroid Influx into the Uterus^*

Departments of Obstetrics and Gynecology and Internal Medicine, University of California, Los Angeles, California 90024

Address requests for reprints to: Howard L. Judd, M.D., UCLA School of Medicine, Department of Obstetrics and Gynecology, University of California, Los Angeles, California 90024.

To determine the effect of such factors as capillary membrane permeability, plasma protein binding, and capillary transit time on the availability of sex steroids to the uterus, the unidirectional influxes of ³H-labeled steroids from the circulation into the uterus were measured in vivo in anesthetized rats using a tissue-sampling, single injection technique. When dihydrotestosterone (DHT), estradiol (E₂), and progesterone (P) were injected with Ringer's solution, the tissue extraction was in excess of 80%; hence, membrane permeability did not play a limiting role. With the more polar steroids, corticosterone and cortisol, uterine extraction was less than 40%.

Significant inhibition of tissue extraction of DHT and E₂, but not P, occurred with the addition of 4% albumin to the injection solution. Human sera containing increasing concentrations of sex hormone-binding globulin demonstrated inhibition of extraction of DHT and E₂. Human sera also inhibited P extraction, presumably secondary to the presence of cortisol-binding globulin and orosomucoid.

Large concentrations of unlabeled DHT, E₂, and P in the injection solutions did not result in competitive inhibition of labeled steroid extraction. Thus, there is no evidence for a carrier mechanism mediating steroid transport into the uterus.

When tissue extraction of E₂ from Ringer's solution was compared in liver, brain, and uterus, no difference of tissue permeability could be found. Liver consistently had higher tissue E₂ extraction than brain or uterus in the presence of human sera. The results are compatible with the influx of albuminbound E₂ into all three tissues and the influx of sex hormonebinding globulin-bound E₂ into the liver. (J Clin Metab 56:1282, 1983)

^* This work was supported in part by NIH Grants CA-23093 and AM-25744 and Research Career Development Award AM-00782 (to W.M.P.).

Received July 6, 1982.