Ovarian Dysfunction Induced by Chronic Whole-Body PM2.5 Exposure

Area of Science:

• Environmental Health
• Reproductive Biology
• Toxicology

Background:

• Fine particulate matter (PM2.5) poses global health risks.
• Epidemiological data links PM2.5 exposure to increased female infertility.
• Limited research systematically investigates chronic PM2.5 effects on ovarian function and mechanisms.

Purpose of the Study:

• To explore the impact of chronic PM2.5 exposure on female mouse ovarian function.
• To elucidate the underlying molecular mechanisms of PM2.5-induced ovarian damage.
• To evaluate the protective potential of dietary polydatin (PD) against PM2.5 toxicity.

Main Methods:

• Female C57BL/6J mice were exposed to filtered air or PM2.5 for 4 months.
• Estrus cycles, reproductive parameters, hormone levels, and ovarian reserve were assessed.
• RNA sequencing identified gene expression changes, focusing on key pathways.
• Mitochondria-dependent apoptosis, oxidative stress, inflammation, and NF-κB/IL-6 signaling were investigated.

Main Results:

• PM2.5 exposure significantly altered estrus cycles, reproductive capacity, hormone levels, and ovarian reserve.
• Granulosa cell apoptosis via the mitochondria-dependent pathway contributed to follicle atresia.
• RNA-seq revealed enrichment in steroidogenesis, reactive oxygen species, and oxidative phosphorylation pathways.
• PM2.5 exacerbated ovarian oxidative stress and inflammation through the NF-κB/IL-6 pathway.
• Dietary polydatin (PD) demonstrated a protective effect against PM2.5-induced ovarian dysfunction.

Conclusions:

• Chronic PM2.5 exposure is a critical factor in ovarian dysfunction.
• Mechanisms involve mitochondria-dependent apoptosis and NF-κB/IL-6-mediated inflammation and oxidative stress.
• Polydatin (PD) may be a potential therapeutic candidate for air pollution-related ovarian dysfunction.