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In HBECs, the increase in ROS levels triggered by CSE exposure was likely a key factor leading to the translocation of Drp1 to the mitochondria and subsequent induction of mitochondrial fission, and effective inhibition of Drp1 translocation and mitochondrial fragmentation by the ROS scavenger N-acetylcysteine (NAC) supported this view (Hara et al., 2013)