Cao Nannan, Hu Chunhui, Xia Bintong, He Yan, Huang Jiaolong, Yuan Zhicheng, Deng Jie, Duan Peng
Postgraduate Union Training Base of Jinzhou Medical University, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000 Hubei Province, China.
Key Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases of Xiangyang City, Department of Obstetrics and Gynaecology, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000 Hubei Province, China.
Oxid Med Cell Longev. 2022 Jun 8;2022:4240490. doi: 10.1155/2022/4240490. eCollection 2022.
Asthenozoospermia is a common form of abnormal sperm quality in idiopathic male infertility. While most sperm-mediated causes have been investigated in detail, the significance of seminal plasma has been neglected. Herein, we aimed to investigate the possible pathogenic factors leading to decreased sperm motility based on seminal plasma. Semen was collected from normo- (NOR, = 70), idiopathic oligo- (OLI, = 57), and idiopathic asthenozoospermic (AST, = 53) patients. Using attenuated total reflection-Fourier transform infrared coupled with chemometrics, distinct differences in the biochemical compositions of nucleic acids, protein structure (amides I, II, and III), lipids, and carbohydrates in seminal plasma of AST were observed when compared to NOR and OLI. Compared with NOR and OLI, the levels of peptide aggregation, protein phosphorylation, unsaturated fatty acid, and lipid to protein ratio were significantly increased in AST; however, the level of lipid saturation was significantly decreased in seminal plasma of AST. Compared with NOR, the levels of ROS, MDA, 8-iso-prostaglandin F2 (8-isoPGF2), and the ratio of phospho-AMPK/AMPK1 were significantly increased in AST; however, the levels of SOD, glutathione S-transferase (GSTs), protein carbonyl derivative (PC), and the ratio of phospho-Rictor/Rictor were significantly decreased in seminal plasma of AST. Changes of the AMPK/mTORC2 signaling in the seminal microenvironment possibly induce abnormal glucose and lipid metabolism, which impairs energy production. Oxidative stress potentially damages seminal plasma lipids and proteins, which in turn leads to impaired sperm structure and function. These findings provide evidence that the changes in seminal plasma compositions, oxidative stress, and activation of the AMPK/mTORC2 signaling contribute to the development of asthenozoospermia.
弱精子症是特发性男性不育中常见的精子质量异常形式。虽然大多数精子介导的病因已得到详细研究，但精浆的重要性却被忽视了。在此，我们旨在基于精浆研究导致精子活力下降的可能致病因素。从正常（NOR，n = 70）、特发性少精子症（OLI，n = 57）和特发性弱精子症（AST，n = 53）患者中收集精液。使用衰减全反射 - 傅里叶变换红外光谱结合化学计量学方法，与NOR和OLI相比，观察到AST患者精浆中核酸、蛋白质结构（酰胺I、II和III）、脂质和碳水化合物的生化组成存在明显差异。与NOR和OLI相比，AST患者精浆中肽聚集、蛋白质磷酸化、不饱和脂肪酸水平以及脂质与蛋白质的比率显著升高；然而，AST患者精浆中脂质饱和度水平显著降低。与NOR相比，AST患者精浆中活性氧（ROS）、丙二醛（MDA）、8 - 异前列腺素F2（8 - isoPGF2）水平以及磷酸化腺苷酸活化蛋白激酶（AMPK）/AMPK1的比率显著升高；然而，AST患者精浆中超氧化物歧化酶（SOD）、谷胱甘肽S - 转移酶（GSTs）、蛋白质羰基衍生物（PC）水平以及磷酸化雷帕霉素靶蛋白复合物2（Rictor）/Rictor的比率显著降低。精浆微环境中AMPK/mTORC2信号通路的变化可能诱导异常的葡萄糖和脂质代谢，从而损害能量产生。氧化应激可能损害精浆中的脂质和蛋白质，进而导致精子结构和功能受损。这些发现提供了证据，表明精浆成分的变化、氧化应激以及AMPK/mTORC2信号通路的激活促成了弱精子症的发生。
