Bromuconazole fungicide induces cell cycle arrest and apoptotic cell death in cultured human colon carcinoma cells (HCT116) via oxidative stress process

Autor:	Karima, Rjiba-Touati, Imen, Ayed-Boussema, Hiba, Hamdi, Awatef, Azzebi, Salwa, Abid
Rok vydání:	2022
Předmět:	Caspase 3 Colon Superoxide Dismutase Health Toxicology and Mutagenesis Carcinoma Clinical Biochemistry Apoptosis Cell Cycle Checkpoints DNA Triazoles Biochemistry Fungicides Industrial Acetylcysteine Oxidative Stress Cell Line Tumor Humans Reactive Oxygen Species Fluorescein-5-isothiocyanate Biomarkers
Zdroj:	Biomarkers. 27:659-670
ISSN:	1366-5804 1354-750X
DOI:	10.1080/1354750x.2022.2098378
Popis:	Bromuconazole, a fungicide belonging to the triazole family, is a plant protection product used to control, repel or destroy fungi that may develop on crops. We investigated the pro-apoptotic effect of bromuconazole and the role of oxidative stress in the death mechanism induced by this fungicide in this study.The human colon HCT116 cell line was treated with Bromuconazole (IC50/4, IC50/2, and IC50) for 24 h. Cells were collected and analysed for biomarkers of apoptotic cell death and oxidative stress as well as for the assessment of genotoxic damage.Our study showed that bromuconazole caused a concentration-dependent increase in cell mortality with an IC50 of 180 µM. Bromuconazole induced cell cycle arrest in the G0/G1 phase and DNA synthesis inhibition. The Comet assay showed that bromuconazole caused DNA damage in a concentration-dependent manner. Bromuconazole-induced apoptosis was observed by, Annexin-V/FITC-PI and BET/AO staining, by mitochondrial membrane depolarisation, and by increased caspase-3 activity. In addition, bromuconazole induced a significant increase in ROS and lipid peroxidation levels and a disruption in SOD and CAT activities. N-acetylcysteine (NAC) strongly prevents cytotoxic and genotoxic damage caused by bromuconazole.Bromuconazole toxicity was through the oxidative stress process, which causes DNA damage and mitochondrial dysfunction, leading to cell cycle arrest and apoptotic death of HCT116 cells.Bromuconazole exposure induced cell cycle arrest in the G0/G1 in HCT116 cells.Bromuconazole caused DNA synthesis inhibition and degradation.Bromuconazole-induced Annexin-V/FITC-PI and BET/AO positive staining, increased caspase-3 activity and MMP.Bromuconazole enhances ROS, MDA levels and disruption of CAT and SOD activities.
Databáze:	OpenAIRE
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