Department of Dermatology, Venereology and Andrology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt.
Department of Clinical and Chemical Pathology, Faculty of Medicine, University of Alexandria, Alexandria, Egypt.
Andrologia. 2021 Oct;53(9):e14172. doi: 10.1111/and.14172. Epub 2021 Jul 1.
Vitamin D deficiency has been linked with different health problems including male infertility. Its function is mediated by the vitamin D receptor, which acts as a transcription factor. Epigenetic mechanisms such as DNA methylation may affect the vitamin D receptor gene and result in gene silencing. The present study aimed to assess serum vitamin D level and seminal methylation of vitamin D receptor gene in idiopathic male infertility. Blood and semen samples were collected from 60 men with idiopathic infertility and 40 healthy fertile men. Vitamin D levels were detected using enzyme-linked fluorescent assay technique and methylation status was assessed by methylation-specific PCR. Results revealed that serum levels of 25OHD were significantly lower in patients compared to controls. Positive correlation was found between serum level of 25OHD and sperm concentration in patients group and progressive motility in total studied group. Methylation of vitamin D receptor gene was significantly higher in patients compared to control group. Negative correlation was found between methylation of vitamin D receptor gene and both sperm concentration and progressive motility in total studied group. Results of the present study suggest that vitamin D deficiency and vitamin D receptor gene methylation may be involved in aetiopathogenesis of idiopathic male infertility.
维生素 D 缺乏与多种健康问题有关，包括男性不育。其功能是由维生素 D 受体介导的，维生素 D 受体作为转录因子发挥作用。表观遗传机制，如 DNA 甲基化，可能会影响维生素 D 受体基因，导致基因沉默。本研究旨在评估特发性男性不育症患者血清维生素 D 水平和维生素 D 受体基因的精液甲基化。采集了 60 名特发性不育男性和 40 名健康生育男性的血液和精液样本。采用酶联荧光检测技术检测维生素 D 水平，采用甲基化特异性 PCR 评估甲基化状态。结果显示，与对照组相比，患者的血清 25OHD 水平明显降低。患者组血清 25OHD 水平与精子浓度呈正相关，总研究组与前向运动精子活力呈正相关。与对照组相比，患者的维生素 D 受体基因甲基化明显升高。维生素 D 受体基因甲基化与总研究组的精子浓度和前向运动精子活力均呈负相关。本研究结果表明，维生素 D 缺乏和维生素 D 受体基因甲基化可能参与特发性男性不育症的发病机制。
