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Journal of Andrology, Vol 18, Issue 4 411-416, Copyright © 1997 by The American Society of Andrology

JOURNAL ARTICLE

HCG binding to the testicular LH receptor is similar in fertile, subfertile, and infertile stallions

D. D. Motton and J. F. Roser
Department of Animal Science, University of California, Davis 95616, USA.

Recent evidence in our laboratory suggests that the cause of idiopathic subfertility/infertility in breeding stallions may originate in the testes at the luteinizing hormone (LH) receptor or postreceptor level. The objective of this research was to determine if LH receptor binding activity is altered in subfertile and infertile stallions. Six fertile, three subfertile, and three infertile stallions, ages 11-23 years, were classified according to normal semen parameters and pregnancy rates and then castrated in the breeding season. Blood was collected prior to castration, and plasma was stored until analyzed for LH, follicle stimulating hormone (FSH), estrogen conjugates (EC), estradiol (E2), testosterone (T), and inhibin (I) by radioimmunoassay (RIA). Testicular cell membranes were prepared and snap-frozen until analyzed for LH binding activity by radioreceptorassay (RRA) using increasing amounts of I125 human chorionic gonadotropin (hCG). Luteinizing hormone receptor numbers and affinity constants were determined by Scatchard analysis. Plasma LH, FSH, EC, E2, and T levels did not differ between fertile and subfertile stallions, but LH and FSH were significantly higher (P < 0.05) and EC, E2, T, and I levels were significantly lower (P < 0.05) in infertile stallions as compared to fertile and subfertile stallions. Receptor number (Rt) and affinity constants Ka were similar (P > 0.05) between fertile (Rt = 9.44 x 10(-11) M, Ka = 0.300 x 10(10) M-1), subfertile (Rt = 13.02 x 10(-11) M, Ka = 0.194 x 10(10) M-1), and infertile (Rt = 7.65 x 10(-11) M, Ka = 0.380 x 10(10) M-1) stallions. In conclusion, these data suggest that an endocrine dysfunction in the testes of stallions with poor fertility may not be due to a LH receptor disorder but may be due to a postreceptor malfunction.


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M. Saint-Dizier, F. Foulon-Gauze, F. Lecompte, Y. Combarnous, and M. Chopineau
Cloning and functional expression of the equine luteinizing hormone/chorionic gonadotrophin receptor
J. Endocrinol., December 1, 2004; 183(3): 551 - 559.
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Copyright © 1997 by The American Society of Andrology.