[Back to Number 10 ToC] [Back to Journal Contents] [Back to Biokhimiya Home page]
[View Full Article] [Download Reprint (PDF)]

Luteinizing Hormone-Releasing Hormone in Thymus and Hypothalamus of Rat Fetuses: Suppressing Effect of Antagonist and of Antibodies on Concanavalin A-Induced Proliferation of Thymocytes

L. A. Zakharova1*, I. V. Malyukova1, E. I. Adamskaya2, T. A. Kuznetsova2, and I. V. Shishkina2

1Kol'tsov Institute of Developmental Biology, Russian Academy of Sciences, ul. Vavilova 26, Moscow, 117871 Russia; fax: (095) 135-8012; E-mail: zaharova@ibrran.msk.su

2Endocrinology Research Center, Russian Academy of Medical Sciences, ul. Dmitriya Ul'yanova 11, Moscow, 117036 Russia

* To whom correspondence should be addressed.

Received March 9, 2000; Revision received May 10, 2000
The effect of endogenous luteinizing hormone-releasing hormone (LHRH) on the proliferation induced by concanavalin A (Con A) in rat fetal thymocytes was studied. A selective antagonist (2 µg per fetus) or antibodies to LHRH (20 µl per fetus) were injected in utero into 20-day-old rat fetuses, and this resulted in a two- or fivefold decrease in the Con A-induced proliferation of thymocytes, respectively. In combined culture of the antagonist (10-5-10-6 M) with fetal thymocytes, the proliferative response was not decreased. The concentration of LHRH was determined by radioimmunoassay in tissues of immunocompetent organs and in blood serum of 18- and 21-day-old fetuses, and the hormone was found in the hypothalamus, thymus, and peripheral blood. The initially low level of LHRH in the thymus increased by 65 and 40%, respectively, on the first day after birth and became similar to the level in the hypothalamus. In the fetal blood serum, the LHRH level was significantly higher than in the thymus and hypothalamus of fetuses of the same age. The hormone concentration was greatest in the 18-day-old fetuses, and it decreased twofold by the 21st day. The findings indicate that LHRH is involved in regulation of T-cell immunity even during prenatal ontogenesis.
KEY WORDS: LHRH, antibodies, thymus, hypothalamus, radioimmunoassay, proliferative response, prenatal ontogenesis