Wang Cao, Zhao Yingchi, Liu Bin, Luo Zhen, Zhou Guangxu, Mao Kaiyi
Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou province, China.
Guizhou Children's Hospital, Zunyi, Guizhou province, China.
PLoS One. 2025 Apr 2;20(4):e0313803. doi: 10.1371/journal.pone.0313803. eCollection 2025.
To 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.
In 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).
After 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 < 0.05), increased expressions of malondialdehyde (MDA), Bcl-2 associated X protein (Bax), and Caspase3 (p < 0.05), and downregulated expressions of C/EBP homologous protein (CHOP), heat shock protein 60 (HSP60), and activating transcription factor 5 (ATF5) (p < 0.05). These were all reversed by vitamin intervention.
PM2.5 from automobile exhaust disrupts male reproductive function. A combination of vitamins may protect reproductive function via the reactive oxygen species (ROS)-UPRmt signaling pathway.
探讨细颗粒物(PM2.5)介导的雄性大鼠生殖功能调节的潜在机制,并确定维生素在此过程中的作用。
将32只雄性SD大鼠随机分为对照组(生理盐水)、维生素组(100mg/kg维生素C + 50mg/kg维生素E)、PM2.5组(10mg/kg PM2.5)和PM2.5 + 维生素组(PM2.5暴露 + 100mg/kg维生素C + 50mg/kg维生素E),每组8只大鼠。暴露4周后进行交配实验。此后,对大鼠实施安乐死,并切除睾丸和附睾组织进行苏木精-伊红(HE)染色和精子质量分析。通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)法对睾丸组织的凋亡进行定量。此外,通过蛋白质免疫印迹法(WB)检测睾丸氧化应激(OS)、凋亡和线粒体未折叠蛋白反应(UPRmt)相关的关键蛋白表达。
PM2.5暴露后,精子数量和活力下降,而精子畸形率和凋亡指数增加。HE染色显示生精细胞数量减少。WB显示,PM2.5组超氧化物歧化酶(SOD)、核因子E2相关因子2(Nrf2)和B细胞淋巴瘤-2(Bcl-2)的表达降低(p < 0.05),丙二醛(MDA)、Bcl-2相关X蛋白(Bax)和半胱天冬酶3(Caspase3)的表达增加(p < 0.05),C/EBP同源蛋白(CHOP)、热休克蛋白60(HSP60)和激活转录因子5(ATF5)的表达下调(p < 0.05)。这些变化均被维生素干预逆转。
汽车尾气中的PM2.5破坏雄性生殖功能。维生素组合可能通过活性氧(ROS)-UPRmt信号通路保护生殖功能。