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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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Bibliographic Details
Published in:Cell biology international 2017-03, Vol.41 (3), p.309
Main Authors: Akcakaya, Handan, Tok, Sabiha, Dal, Fulya, Cinar, Suzan Adin, Nurten, Rustem
Format: Article
Language:English
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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.
ISSN:1065-6995
1095-8355
DOI:10.1002/cbin.10727