Functional melatonin receptors in human prostate epithelial cells

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Published on Wednesday, 01 April 2020

Abstract

Melatonin, secreted nocturnally by the pineal gland, affects gonadal growth and pubertal development in rodents and, presumably, in humans.

Recently, we have found, using 125I-labeled melatonin as a probe, specific melatonin binding sites in the human benign prostate tissue; these sites were primarily associated with the microsomal fraction of the epithelial cells.

In the present study, we have explored 125I-melatonin binding sites in human benign prostate epithelial cells in culture and investigated the effects of melatonin on growth and viability of these cells. 125I-melatonin bound to the prostate cells with high (K(d) = 68 pM) affinity. Competition experiments revealed that specific binding was inhibited by subnanomolar concentrations of melatonin and 2-iodomelatonin, whereas serotonin and 5-methoxytryptamine reduced the binding only partially.

Melatonin (10 pM-10 nM) inhibited the incorporation of 3H-thymidine and 3H-uridine into the prostate epithelial cells in a dose-dependent manner. Inhibition was transient, and the incorporation recovered to control levels within less than 24 h. Protein synthesis as measured by the incorporation of 35S-methionine into cell proteins decayed to minimal levels about 2 h after addition of melatonin, and its recovery was slower compared with that of 3H-thymidine or 3H-uridine incorporation. Melatonin treatment (1 nM) for 2-7 days inhibited cell growth and markedly increased the percentage of non-viable cells in culture, measured by the trypan blue exclusion assay.

The results demonstrate high affinity melatonin receptors in the human benign prostate epithelial cells, which may affect cell growth and viability.

 



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- About Melatonin - In vitro, review and in vivo publications;

- Publication: Melatonin anticancer effects: Review (from Di Bella's Foundation);

- Publication: Key aspects of melatonin physiology: 30 years of research (from Di Bella's Foundation);

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