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Singlet Oxygen Toxicity Is Cell Line‐dependent: A Study of Lipid Peroxidation in Nine Leukemia Cell Lines
Author(s) -
Schafer Freya Q.,
Buettner Garry R.
Publication year - 1999
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1999.tb08294.x
Subject(s) - lipid peroxidation , singlet oxygen , toxicity , leukemia , cell culture , chemistry , oxygen toxicity , cell , oxygen , photochemistry , biochemistry , biology , oxidative stress , immunology , genetics , organic chemistry
Abstract Singlet oxygen ( 1 O 2 ) can be quenched by water, lipids, proteins, nucleic acids and other small molecules. Polyunsaturated fatty acids (PUFA) of cells principally quench 1 O 2 by chemical mechanisms, producing lipid hydroperoxides, while proteins physically and chemically quench 1 O 2 . Because cell lines can have different PUFA and protein levels, we hypothesized that 1 O 2 toxicity will vary between cell lines. We used Photofrin® as a source of 1 O 2 . Exposure of nine different leukemia cell lines (CEM, HEL, HL‐60, K‐562, KG‐1, L1210, Molt‐4, THP‐1 and U‐937) to Photofrin and light results in changes in membrane permeability (trypan blue) that vary with cell line. The greater the lipid content of the cell line, the less susceptible they are to membrane damage. When the cell media was supplemented with docosahexaenoic acid (DHA, 22:6), the overall unsaturation of cellular lipids increased. Photofrin and light resulted in increased radical formation in these supplemented cells compared to controls; however, there was no difference in membrane permeability between DHA‐supplemented and control cells. Lipid‐derived radical formation (electron paramagnetic resonance spin trapping) was cell line dependent; but no correlation between lipid content of cells and radical formation was found. However, we found that the greater the protein content of cells the more they were protected against membrane damage induced by Photofrin photosensitization. This suggests that cellular proteins are a key target for 1 O 2 ‐mediated toxicity. A remarkable observation is that cell size correlates inversely with ability of cells to cope with a given flux of 1 O 2 .

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