Pineal Research Lab, Department of Zoology, Banaras Hindu University, Varanasi 221005, India.
Endocrine. 2010 Jun;37(3):479-88. doi: 10.1007/s12020-010-9331-7. Epub 2010 Apr 13.
Local antigonadotrophic action of melatonin in testes has never been correlated with local and general immune status of any rodent. Intra-testicular injection of melatonin (2.5 μg/50 μl) for 10 days (MI-10D) and 20 days (MI-20D) was given to young adult male of Funambulus pennanti and testicular androgen receptor (AR), androgen binding protein (ABP) expression, 3β-hydroxysteroid dehydrogenase (3β-HSD) activity, and Mel1aR expression in thymus was checked along with general immune parameters. Further, immunohistochemical localization of Mel1aR in testes was done. Decreased AR, ABP expression, testes weight, 3β-HSD activity, testosterone level, and spermatogenesis but increased Mel1aR expression in thymus, immunoreactivity in testes, and testicular macrophages following injection was noted. Lymphatic tissue weight, leukocyte, lymphocyte count, lymphocyte proliferation in spleen, thymus, plasma melatonin, and IL-2 level increased in a duration-dependent manner following intra-testicular injection. Intra-testicular injection of melatonin decreased steroidogenesis by enhancing the primary effect of melatonin on Leydig cell endocrine function. Along with reduced circulatory testosterone production, an increase in testicular as well as general immunity was observed in a duration-dependent manner. Therefore, a local participation of melatonin in testes of F. pennanti to control testicular androgen production is suggested.
褪黑素在睾丸中的局部抗促性腺作用从未与任何啮齿动物的局部和全身免疫状态相关联。将褪黑素(2.5μg/50μl)注射到成年雄性金线蛙的睾丸中 10 天(MI-10D)和 20 天(MI-20D),检查睾丸雄激素受体(AR)、雄激素结合蛋白(ABP)表达、3β-羟类固醇脱氢酶(3β-HSD)活性和胸腺中的 Mel1aR 表达,以及一般免疫参数。此外,还进行了 Mel1aR 在睾丸中的免疫组织化学定位。注射后,胸腺中的 Mel1aR 表达、睾丸中的免疫反应性和睾丸巨噬细胞增加,但 AR、ABP 表达、睾丸重量、3β-HSD 活性、睾酮水平和精子发生减少。淋巴组织重量、白细胞、淋巴细胞计数、脾、胸腺淋巴细胞增殖、血浆褪黑素和 IL-2 水平在睾丸内注射后呈时间依赖性增加。褪黑素的睾丸内注射通过增强褪黑素对间质细胞内分泌功能的主要作用来降低类固醇生成。随着循环睾酮产生的减少,睾丸和全身免疫力呈时间依赖性增加。因此,建议褪黑素在金线蛙睾丸中局部参与控制睾丸雄激素的产生。