Indomethacin decreases both luteinizing hormone binding and fluidity of testicular microsomal membranes in rat.

The objective of these studies was to examine the effects of in vivo treatment with indomethacin, a prostaglandin synthesis inhibitor, on luteinizing hormone receptors and fluidity in microsomal membrane preparations of rat testis. Adult male rats were treated with vehicle or either of two doses of indomethacin (3.8 micrograms/g body weight or 7.5 micrograms/g body weight) every 8 h for 1, 2 and 3 days. Indomethacin treatment decreased human luteinizing hormone (hLH) binding in rat testis in a time-dependent fashion. The lower dose of indomethacin decreased hLH binding by 19%, 35% and 50%, respectively, after 1, 2 and 3 days of treatment. The higher dose of indomethacin decreased hLH binding at these respective times by 21%, 44% and 56%. Scatchard analysis of the hLH binding of testicular membrane preparations indicated that indomethacin treatment decreased the number of hLH binding sites rather than the apparent affinity constant. Testicular membrane fluidity was estimated by a fluorescence polarization technique. The effects of indomethacin on apparent fluidity of microsomal membrane paralleled that of LH binding. The values of apparent microviscosity, inversely related to the fluidity, also increased in a time-dependent fashion. These simultaneous effects of indomethacin on testicular LH binding and fluidity suggest that these phenomena are interrelated and that prostaglandins are involved in the maintenance of LH receptors in vivo.