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- W2003672112 abstract "Melatonin, secreted by the pineal gland at night, inhibits pubertal development of rats and presumably men. In addition, it may directly suppress prostate growth in the adult rat. To investigate the possibility for a causal relationship between the age-related decline in melatonin production and increase in prevalence of benign prostate hypertrophy (BPH) in man, the presence of melatonin binding sites in human BPH tissue was examined. In vitro autoradiography indicated specific 125I-labeled melatonin (125I-melatonin) binding in the prostate, localized to the glandular epithelium. Separation and subcellular fractionation indicated that these sites were associated with the microsomal fraction of the epithelial cells. Kinetic and equilibrium 125I-melatonin binding experiments revealed that the binding was time dependent and reversible, with an apparent half saturation at 140 pmol/L. Competition experiments indicated high and low affinity melatonin binding sites; binding was inhibited by melatonin (IC50 1 nmol/L and 1 micromol/L, respectively) and partially by the putative melatonin antagonist, N-(2,4 dinitrophenyl)-5-methoxytryptamine (ML-23; IC50 0.1 nmol/L). Serotonin and 6-hydroxymelatonin were less potent, whereas up to 0.1 mmol/Lol/L of 5-methoxytryptamine, 6-methoxymelatonin, and tryptamine caused only a partial reduction in specific binding. The guanine nucleotide analogs, guanosine 5'-O-[3-thiotriphosphate] and guanosine 5'-O-[2-thio-diphosphate, inhibited specific 125I-melatonin binding, whereas 5'-guanylyl imidodiphosphate was less potent. The results indicate putative melatonin receptors in the human prostate epithelium." @default.
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- W2003672112 title "Putative melatonin receptors in benign human prostate tissue." @default.
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- W2003672112 doi "https://doi.org/10.1210/jcem.81.4.8636329" @default.
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