Appraisal of time-dependent ros-mediated mitochondrial damage induced by arsenic and its alleviation by catechin in epithelial cells

Mitochondria play an important role in cellular energetics and balance. High levels of reactive oxygen species induce oxidative stress in living cells. Arsenic is known to induce reactive oxygen species (ROS), and oxidative stress is the major cause of mitochondrial impairment leading to cell death. It also explains the preneoplastic events and cancer of the bladder. Polyphenols are known to forestall chronic disorders. Catechins (flavan-3-ols) are a subgroup of flavonoids. Here in the current study to evaluate the amelioration of arsenate-induced cytotoxicity by catechin, parameters such as ROS, mitochondrial membrane potential (MMP) apoptosis, and DNA damage were considered and evaluated in epithelial cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay was performed to evaluate cell viability. ROS was measured at different time points (30 min, 1 h, and 2 h) to ensure the quenching activity of catechin. Pre-treatment of the cells with catechin ameliorated arsenic-induced cytotoxicity in epithelial cells and the results were significant (p < 0.05).