| Popis: |
Although numerous studies have investigated that atmospheric fine particulate matter (PM2.5) can be toxic to environmental organisms, the research on the reproductive toxicity of PM2.5 is limited, and the key toxic components and underlying mechanisms remain unknown. In this work, PM2.5 samples of four seasons in Nanjing from March 1, 2021, to February 28, 2022 were collected and the chemical components were analyzed. Caenorhabditis elegans (C. elegans) was employed to conduct the toxicological testing. The reproductive toxicity of PM2.5 to C. elegans in different seasons was evaluated by multiple reproductive endpoints. Exposure to high concentrations of PM2.5 significantly decreased the brood size and the number of fertilized eggs in utero. PM2.5 exposure also increased the number of germ cell corpses and caused abnormal expression of apoptosis-related genes (ced-9, ced-4, and ced-3), which confirmed that PM2.5 induced germline apoptosis. In addition, PM2.5 exposure significantly increased the production of reactive oxygen species (ROS) in C. elegans and the fluorescence intensity of HUS-1 protein in of transgenic strain WS1433. Meanwhile, the expression of genes related to DNA damage (cep-1, clk-2, egl-1, and hus-1) and oxidative stress (mev-1, isp-1, and gas-1) also significantly altered in C. elegans, suggesting induction of DNA damage and oxidative stress. According to Pearson correlation analyses, DNA damage and oxidative stress were significantly correlated with multiple reproductive endpoints in C. elegans. Thus, it was speculated that PM2.5 caused reproductive dysfunction and germ cell apoptosis in C. elegans may be by inducing ROS and DNA damage. In addition, heavy metals in PM2.5 were significantly correlated with multiple endpoints at physiological and biochemical, suggesting that the heavy metals might be an important contributor to the reproductive toxicity induced by PM2.5. |
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