The reproductive toxicology of male SD rats after PM2.5 exposure mediated by the stimulation of endoplasmic reticulum stress

- PM2.5 exposure caused toxicity of sperm in SD male rats.
- PM2.5 could lead to toxicity of reproductive tissue in SD male rats.
- PM2.5 exposure activated ERS-mediated apoptosis of reproductive tissue through the up-regulation of CHOP and Caspase-12.
- Reproductive toxicity of Winter PM2.5 was greater than that of summer PM2.5 in Taiyuan city.

Evidence has shown that exposure to fine particulate matter (PM) contributed to poor semen quality in males. However, the reproductive toxicity and relevant molecular mechanisms of Particular Matter 2.5 (PM2.5) from different seasons are not well understood. In the present work, we intend to investigate the toxic effects of PM2.5 during summer and winter on reproductive cells and tissues and focus on endoplasmic reticulum stress (ERS) to illustrate the possible molecular mechanisms. Sprague Dawley (SD) rats were exposed to PM2.5 from the summer season (0.2, 0.6, and 1.5 mg/kg b. w.) and winter (0.3, 1.5, and 2.7 mg/kg b. w.) through intratracheal instillation. The exposure was performed once every 3 days and continued for 2 months. Sperm and reproductive organs (testis and epididymis) were collected from the animals to conduct toxicity evaluation and mechanism analysis. The data showed that sperm relative motility rates were remarkably decreased, while sperm malformation rates were significantly increased with exposure to the summer and winter PM2.5. In particular, the reproductive toxicity of winter PM2.5 in the highest dose group was significantly greater than that in the other PM2.5 exposure groups. The pathological results also showed that the rats in the winter PM2.5 group of 2.7 mg/kg b. w. had severe testicular tissue injury, as determined by haematoxylin and eosin (HE) staining. The apoptotic results obtained by terminal dUTP nick-end labelling (TUNEL) further suggested that summer and winter PM2.5 exposure promoted the testicular germ cell apoptosis. The reproductive toxicity of winter PM2.5 in the testis was stronger than that of summer PM2.5. In addition, the expressions of GRP78 and XBP-1, biomarkers of ERS, was enhanced under the conditions of PM2.5 exposure, and ERS-mediated apoptosis through the upregulation of CHOP and Caspase-12 in the epididymis and testis was activated. In conclusion, PM2.5 exposure induced reproductive toxicity in male SD rats by the stimulation of ERS.