Toxicity mechanism of acrolein on DNA damage and apoptosis in BEAS-2B cells: Insights from cell biology and molecular docking analyses
Abstract
Acrolein induced DNA damage and nucleus condensation in BEAS-2B cells. Acrolein activated DNA damage response, and caused cell cycle arrest in G2/M phase. The spontaneous binding of acrolein with DNA was revealed by molecular docking. Acrolein induced BEAS-2B cell apoptosis by the mitochondrial apoptotic pathway.
- Publication:
-
Toxicology
- Pub Date:
- January 2022
- DOI:
- 10.1016/j.tox.2021.153083
- Bibcode:
- 2022Toxgy.46653083L
- Keywords:
-
- BEAS-2B cells;
- human bronchial epithelial cells;
- DMSO;
- dimethyl sulfoxide;
- MTT;
- 3‑4 5-dimethylthiazol-2-yl)-2;
- 5-diphenyltetrazolium bromide;
- MMP;
- mitochondrial membrane potential;
- ATP;
- adenosine triphosphate;
- OTM;
- olive tail moment;
- EB;
- ethidium bromide;
- CASP;
- comet assay software project;
- PBS;
- phosphate buffered saline;
- V-FITC;
- V-fluorescein isothiocyanate;
- PI;
- propidium iodide;
- PVDF;
- polyvinylidene fluoride;
- SD;
- standard deviation;
- ANOVA;
- analysis of variance;
- DDR;
- DNA damage response;
- ATM;
- Ataxia-telangiectasia-mutated;
- ATR;
- Ataxia-telangiectasia-mutated and Rad-3-related;
- DSB;
- double-strand breaks;
- Chk1;
- Checkpoint kinases 1;
- Chk2;
- Checkpoint kinases 2;
- Acrolein;
- DNA damage;
- Cell cycle arrest;
- Molecular docking;
- Apoptosis