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Exogenous Hydrogen Sulfide Mitigates Oxidative Stress and Mitochondrial Damages Induced by Polystyrene Microplastics in Osteoblastic Cells of Mice

Disease Markers 2023 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 40 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Qingping Shi, Feihong Chen, Yuanyi Feng, Yangxi Zheng, Ximei Zhi, Wen Wu

Summary

Researchers found that polystyrene microplastics induced oxidative stress, mitochondrial damage, and altered gene expression in mouse bone-forming cells, while exogenous hydrogen sulfide treatment mitigated these toxic effects by modulating key signaling pathways.

Polystyrene microplastics (mic-PS) have become harmful pollutants that attracted substantial attention about their potential toxicity. Hydrogen sulfide (H2S) is the third reported endogenous gas transmitter with protective functions on numerous physiologic responses. Nevertheless, the roles for mic-PS on skeletal systems in mammals and the protective effects of exogenous H2S are still indistinct. Here, the proliferation of MC3T3-E1 cell was analyzed by CCK8. Gene changes between the control and mic-PS treatment groups were analyzed by RNA-seq. The mRNA expression of bone morphogenetic protein 4 (Bmp4), alpha cardiac muscle 1 (Actc1), and myosin heavy polypeptide 6 (Myh6) was analyzed by QPCR. ROS level was analyzed by 2',7'-dichlorofluorescein (DCFH-DA). The mitochondrial membrane potential (MMP) was analyzed by Rh123. Our results indicated after exposure for 24 h, 100 mg/L mic-PS induced considerable cytotoxicity in the osteoblastic cells of mice. There were 147 differentially expressed genes (DEGs) including 103 downregulated genes and 44 upregulated genes in the mic-PS-treated group versus the control. The related signaling pathways were oxidative stress, energy metabolism, bone formation, and osteoblast differentiation. The results indicate that exogenous H2S may relieve mic-PS toxicity by altering Bmp4, Actc1, and Myh6 mRNA expressions associated with mitochondrial oxidative stress. Taken together, this study demonstrated that the bone toxicity effects of mic-PS along with exogenous H2S have protective function in mic-PS-mediated oxidative damage and mitochondrial dysfunction in osteoblastic cells of mice.

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