Abstract

The presence of high-affinity luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors has been reported in porcine, rabbit, rat and human uteri. We have demonstrated binding of [125I]LH to mouse uterus, which was saturable. Scatchard plot analysis indicated Kd to be 1.37 x 10(-10) mol/l and the maximum binding capacity to be 5.24 nmol/kg protein. Attempts have been made to observe the functional relevance of gonadotropin receptor in the mouse uterus. The size and weight of the uterus remarkably decreased as a result of ovariectomy; administration of LH to ovariectomized (OVX) mice significantly increased the uterine weight in comparison to the OVX control (p < 0.01), indicating a direct effect of LH on the uterus. There was a two-fold decrease of uterine ascorbic acid content in LH-treated OVX mice as compared to the intact control. The gain in uterine weight of OVX mice by LH was due to the increase in uterine protein synthesis. The stimulatory effect of LH on OVX mice uterus appears to be mediated via steroid hormones because it significantly augmented uterine mitochondrial steroidogenesis. Since 17 beta-estradiol (E2) is known to stimulate uterine protein synthesis, the circulatory level of E2 was determined in intact, OVX and OVX + LH-treated mice. A fall in the circulatory level of E2 occurred in OVX mice as compared to the control, while treatment of LH for 7 days (three injections) significantly elevated E2 levels in OVX mice (p < 0.001). This higher level of E2 in OVX mice remains unaltered on adrenalectomy, indicating that adrenals are not the source for increased E2 levels.(ABSTRACT TRUNCATED AT 250 WORDS)

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