Journal
CELL BIOLOGY INTERNATIONAL
Volume 41, Issue 3, Pages 309-319Publisher
WILEY
DOI: 10.1002/cbin.10727
Keywords
apoptosis; cancer; cell death; mitochondria; oxidative stress
Categories
Funding
- Istanbul University Department of Scientific Research Projects [3633]
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Oxidizing agents (e.g., H2O2) cause structural and functional disruptions of molecules by affecting lipids, proteins, and nucleic acids. As a result, cellular mechanisms related to disrupted macro molecules are affected and cell death is induced. Oxidative damage can be prevented at a certain point by antioxidants or the damage can be reversed. In this work, we studied the cellular response against oxidative stress induced by H2O2 and antioxidant-oxidant (-carotene-H2O2) interactions in terms of time, concentration, and treatment method (pre-, co-, and post) in K562 cells. We showed that co- or post-treatment with-carotene did not protect cells from the damage of oxidative stress furthermore co- and post-beta-carotene-treated oxidative stress induced cells showed similar results with only H2O2 treated cells. However, -carotene pre-treatment prevented oxidative damage induced by H2O2 at concentrations lower than 1,000 mu M compared with only H2O2-treated and co- and post-beta-carotene-treated oxidative stress-induced cells in terms of studied cellular parameters (mitochondrial membrane potential [Delta psi(m)], cell cycle and apoptosis). Prevention effect of beta-carotene pre-treatment was lost at concentrations higher than 1,000 mu M H2O2 (2-10mM). These findings suggest that beta-carotene pre-treatment alters the effects of oxidative damage induced by H2O2 and cell death processes in K562 cells.
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