Hypochlorous acid-induced modulation of cellular redox status in HeLa cells.
Myeloperoxidase catalyzes the formation of hypochlorous acid (HOCI) via reaction of H2O2 with CI(-) ions. Although HOCI plays a major role in the human immune system by killing bacteria and other invading pathogens, excessive generation of this oxidant causes damage to tissues. Exposure of HeLa cells to HOCI decreased viability, inactivated antioxidant enzymes, damaged mitochondria, and modulated cellular redox status. HOCI also induced significant increases in cellular oxidative damage reflected by lipid peroxidation, protein oxidation, and DNA damage. HOCI-mediated oxidative damage to HeLa cells may perturb the cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant state.
Park
Sin Young
SY
School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Taegu, Korea.
Shin
Seoung Woo
SW
Lee
Su-Min
SM
Park
Jeen-Woo
JW
D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage; D006367:HeLa Cells; D006801:Humans; D006997:Hypochlorous Acid / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008931:Mitochondria, Muscle / Q000187:drug effects; D016877:Oxidants / Q000494:pharmacology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species; D013050:Spectrometry, Fluorescence; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D016877:Oxidants; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D006997:Hypochlorous Acid