Trade‐off expression of melatonin receptor subtypes (Mel1a and Mel1b) and androgen receptor in lung of a tropical bird, Perdicula asiatica

Abstract

The role of circulatory steroid hormone along with melatonin in lung of any seasonally breeding bird has never been explored so far. This could be interesting because steroid hormones are immunosuppressive while melatonin is immunostimulatory in nature. In our present study, we report the effect of exogenous melatonin and testosterone on expression of melatonin receptor subtypes (Mel1a and Mel1b) and androgen receptor in lung of a tropical bird Perdicula asiatica. Birds were collected from vicinity of Varanasi and acclimatized in laboratory with sufficient food and water. The birds were treated with melatonin and testosterone at dose of 25 µg/100 g B.wt./day and 1 mg/100 g B.wt./day, respectively, for 28 days. At the end of the experiment, the birds were sacrificed and lung tissue and blood sample were collected for immunohistochemistry, Western blot analysis and hormonal assay. Testosterone treatment increased circulatory testosterone and upregulated expression of androgen receptors whereas downregulated expression of melatonin receptor subtypes Mel1a and Mel1b. Melatonin administration increased peripheral melatonin and upregulated expression of melatonin receptor subtypes Mel1a and Mel1b while downregulated androgen receptor. Thus, our results suggest that a trade‐off relationship between melatonin and testosterone exists in regulation of their receptors in lung of Perdicula asiatica.

Effect of dihydrotestosterone on melatonin secretion and the expression of melatonin receptors and apoptosis‐related factors in sheep epididymides

“…Therefore, we treated cauda epididymal epithelial cells cultured in vitro with DHT and observed that DHT inhibited MEL secretion and receptor expression in epididymal epithelial cells. Exogenous T has been reported to modulate AR expression and down‐regulate the expression of MEL receptors (Kharwar et al, 2020), whereas MEL secretion increases in patients with gonadotropin deficiency and decreases in patients with hypo‐testosterone and high gonadotropin hypogonadism, suggesting that both gonadotropin and gonadal steroid hormones regulate MEL secretion in human blood (Luboshitzky et al, 1996). DHT, a more potent steroid hormone than T (Marchetti & Barth, 2013; Saartok et al, 1984; Wright et al, 1999), can participate in the physiological regulation of the epididymis by regulating MEL secretion and receptor expression.…”