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[beta]-carotene treatment alters the cellular death process in oxidative stress-induced K562 cells
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...
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Published in: | Cell biology international 2017-03, Vol.41 (3), p.309 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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 ([beta]-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 [beta]-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, [beta]-carotene pre-treatment prevented oxidative damage induced by H2O2 at concentrations lower than 1,000µM 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]ψm], cell cycle and apoptosis). Prevention effect of [beta]-carotene pre-treatment was lost at concentrations higher than 1,000µM 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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ISSN: | 1065-6995 1095-8355 |
DOI: | 10.1002/cbin.10727 |