N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway

Toxicology in Vitro : an International Journal Published in Association with BIBRA
Yu ZhuHong-Chang Lai

Abstract

Bisphenol-A-glycidyl methacrylate (Bis-GMA) released from dental resin materials causes various toxic effects on gingival epithelium. Thus the underlying mechanisms of its cytotoxicity should be elucidated for safety use. One potential cause of cell damage is the generation of reactive oxygen species (ROS) beyond the capacity of a balanced redox regulation. In this study, we found that exposure of human oral keratinocytes (HOKs) to Bis-GMA caused apoptosis and G1/S cell cycle arrest in parallel with an increased ROS level. Moreover, Bis-GMA induced a depletion of mitochondrial membrane potential, an increase in the Bax/Bcl-2 ratio, an activation of caspase-3 and altered expressions of cell cycle-related proteins (p21, PCNA, cyclinD1). Furthermore, the co-treatment of the ROS scavenger N-acetyl cysteine (NAC) obviously attenuated Bis-GMA-induced toxicity. Here we also evaluated the effects of Bis-GMA on the ROS-related PI3k/Akt pathway. We found that Bis-GMA inhibited the phosphorylation of Akt, whereas the amount of phosphorylated Akt was reverted to the control level in the presence of NAC. Our findings suggested that the toxic effects of Bis-GMA were related to ROS production and the antioxidant NAC effectively reduced Bis-GM...Continue Reading

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Citations

Oct 27, 2016·Journal of Biomedical Materials Research. Part a·Yu ZhuHongchang Lai
Oct 14, 2019·Journal of Biomedical Materials Research. Part a·Yu ZhuHong-Chang Lai
Dec 31, 2016·Molecular Medicine Reports·Qi ZhouRenyuan Wang
Mar 14, 2018·Environmental Science and Pollution Research International·Ming LiDaolin Du
Feb 9, 2021·Dental Materials : Official Publication of the Academy of Dental Materials·K SiemerO Polydorou

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