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Mitophagy and apoptosis mediated by ROS participate in AlCl 3 -induced MC3T3-E1 cell dysfunction.
- Source :
-
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association [Food Chem Toxicol] 2021 Sep; Vol. 155, pp. 112388. Date of Electronic Publication: 2021 Jul 07. - Publication Year :
- 2021
-
Abstract
- Aluminum (Al), as a common environmental pollutant, causes osteoblast (OB) dysfunction and then leads to Al-related bone diseases (ARBD). One of the mechanisms of ARBD is oxidative stress, which leads to an increase in the production of reactive oxygen species (ROS). ROS can induce mitochondrial damage, thereby inducing mitophagy and apoptosis. But whether mitophagy and apoptosis mediated by ROS, and the role of ROS in AlCl <subscript>3</subscript> -induced MC3T3-E1 cell dysfunction is still unclear. In this study, MC3T3-E1 cells used 0 mM Al (control group), 2 mM Al (Al group), 5 mM N-acetyl cysteine (NAC) (NAC group), 2 mM Al and 5 mM NAC (Al + NAC group) for 24 h. We found AlCl <subscript>3</subscript> -induced MC3T3-E1 cell dysfunction accompanied by oxidative stress, apoptosis, and mitophagy. While NAC, a ROS scavenger treatment, restored cell function and alleviated the mitophagy and apoptosis. These results suggested that mitophagy and apoptosis mediated by ROS participate in AlCl <subscript>3</subscript> -induced MC3T3-E1 cell dysfunction.<br /> (Copyright © 2021 Elsevier Ltd. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1873-6351
- Volume :
- 155
- Database :
- MEDLINE
- Journal :
- Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
- Publication Type :
- Academic Journal
- Accession number :
- 34242719
- Full Text :
- https://doi.org/10.1016/j.fct.2021.112388