Pregnancy rate of female rats in each group.

ObjectiveTo explore the underlying mechanism behind the fine particulate matter’s (PM2.5)-mediated regulation of reproductive function in male rats, and to determine the role of vitamins in this process.MethodsIn all, 32 male SD rats were randomized to a control cohort (normal saline), a Vit cohort (vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), a PM2.5 cohort (PM2.5 10 mg/kg), and a PM2.5 + Vit cohort (PM2.5 exposure + vitamin C at 100 mg/kg + vitamin E at 50 mg/kg), with eight rats in each cohort. After four weeks of exposure, mating experiments were carried out. Thereafter, rats were euthanized, and the testis and epididymis tissues were excised for hematoxylin-eosin (HE) staining and sperm quality analysis. Apoptosis of testis tissues was quantified via a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the testicular oxidative stress (OS)-, apoptosis- and mitochondrial unfolded protein response (UPRmt)-related essential protein expressions were measured via western blotting (WB).ResultsAfter PM2.5 exposure, the sperm count and motility decreased, while sperm abnormality and the apoptosis index increased. HE staining showed that the number of spermatogenic cells decreased. WB showed that the PM2.5 group had decreased expressions of superoxide dismutase (SOD), nuclear factor E2-related factor 2 (Nrf2), and B-cell lymphoma-2 (Bcl-2) (p p p ConclusionPM2.5 from automobile exhaust disrupts male reproductive function. A combination of vitamins may protect reproductive function via the reactive oxygen species (ROS)-UPRmt signaling pathway.研究目的：本研究旨在探究细颗粒物（PM2.5）介导调控雄性大鼠生殖功能的潜在机制，并明确维生素在该过程中的作用。研究方法：共纳入32只雄性SD大鼠，随机分为4组，分别为对照组（生理盐水）、维生素干预组（维生素C 100mg/kg+维生素E 50mg/kg）、PM2.5暴露组（PM2.5 10mg/kg）以及PM2.5联合维生素干预组（PM2.5暴露+维生素C 100mg/kg+维生素E 50mg/kg），每组8只。暴露干预4周后开展交配实验。随后将大鼠经安乐处死，摘取睾丸与附睾组织，用于苏木精-伊红（HE）染色及精子质量分析。采用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法量化睾丸组织的细胞凋亡水平。此外，通过蛋白质印迹（WB）检测睾丸组织中氧化应激（OS）、细胞凋亡及线粒体未折叠蛋白反应（UPRmt）相关核心蛋白的表达量。研究结果：PM2.5暴露后，大鼠精子计数与活力均下降，而精子畸形率及细胞凋亡指数升高。HE染色结果显示，生精细胞数量减少。蛋白质印迹结果表明，PM2.5组中超氧化物歧化酶（SOD）、核因子E2相关因子2（Nrf2）及B细胞淋巴瘤-2（Bcl-2）的表达水平显著降低（p p p）。研究结论：汽车尾气来源的PM2.5可破坏雄性生殖功能；联合补充维生素可通过活性氧（ROS）-线粒体未折叠蛋白反应（UPRmt）信号通路保护雄性生殖功能。