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

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.