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Increase in Testis Luteinizing Hormone Receptor by Estrogen in Mice Susceptible to Leydig Cell Tumors

Departments of Reproductive Medicine [R. J. N., A. J. W. H.] and Community Medicine [M. B. S.], University of California, San Diego, La Jolla, California 92093

In an investigation comparing two strains of mice (BALB/c, susceptible to estrogen-induced Leydig cell tumors and C3H, resistant to such tumors), we found that the Leydig cell-luteinizing hormone (LH) receptors increase in BALB/c mice and decrease in C3H mice during estrogen treatment. In the BALB/c strain, LH receptor content in the testes of mice treated 1, 2, 4, 6, or 8 weeks with diethylstilbestrol (DES) was 2.4- to 5.4-fold greater than that in the testes of untreated littermates. By 24 weeks of treatment, the receptor number had increased 10-fold. Likewise, two weeks of estradiol benzoate treatment in BALB/c mice resulted in a dose-dependent increase in LH receptor content. In contrast, in C3H mice, DES treatment resulted in a transient initial increase (60%), followed by a time-dependent decrease in testicular LH receptor number: 38 and 17% that of normal by six and eight weeks of treatment, respectively. In both strains of mice, DES-induced changes in ¹²⁵I-labeled human chorionic gonadotropin binding reflected changes in LH receptor number rather than in receptor affinity (3 x 10^-11 M). The testis weights of BALB/c mice remained normal during DES treatment, whereas those of the C3H decreased with time. Sprague-Dawley rats, resistant to estrogen-induced Leydig cell tumors, like C3H mice, also underwent testicular atrophy and lost LH receptors during DES treatment. The present study demonstrates that estrogen treatment induces diametrically opposed change in testicular LH receptor number in the two strains of mice with different susceptibilities to Leydig cell tumorigenesis.

¹ Postdoctoral trainee (NIH Training Grant PHSAM 07044).

² Recipient of NIH Grant CA-21867 from the Department of Health, Education, and Welfare. To whom requests for reprints should be addressed.

Received 5/28/80. Accepted 1/20/81.

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