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Exclusive Free Radical Mechanisms of Cellular Photosensitization
Author(s) -
Aveline Beatrice M.,
Redmond Robert W.
Publication year - 1998
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.1751-1097.1998.tb09680.x
Subject(s) - phototoxicity , chemistry , radical , lipid peroxidation , photochemistry , trypan blue , reactive oxygen species , hydroxyl radical , thiobarbituric acid , biophysics , irradiation , oxygen , biochemistry , apoptosis , oxidative stress , in vitro , organic chemistry , physics , nuclear physics , biology
In order to determine the specific effects of radical‐induced reactions in the absence of complicating excited‐state pathways, four different thiohydroxamic esters and their parent molecule, N ‐hydroxypyridine‐2(1 H )‐thione, have been studied in murine L1210 leukemia cells for their ability to produce photobiological damage. Irradiation (X exc = 355 nm) of cells in the presence of thiopyridone esters, specific photolytic precursors of sulfur‐, carbon‐ and oxygen‐centered radicals, caused toxicity that was unambiguously demonstrated to result from radical photosensitization mechanisms. Cellular morphological changes were observed following irradiation but apoptosis was not found to take place. A good correlation was evident between lipid peroxidation, measured by the thiobarbituric acid method, and phototoxicity, assessed by the trypan blue exclusion assay, indicating that the ester derivatives exert their effects mainly in plasma and/ or subcellular membranes. Irradiation performed under deaerated conditions also induced significant phototoxicity but the effects of deaeration were dependent on the ester used and are discussed in terms of the nature of the primary radical species generated in each case. Irradiation of L1210 cells in the presence of N ‐hydroxypyridine‐2(1 H )‐thione, a nonspecific, photochemical source of hydroxyl radical, was also found to trigger phototoxicity and lipid peroxidation. However in this case, photodamage cannot yet be definitely attributed to a radical or type II mechanism although the apparent oxygen independence of phototoxicity would indicate that type II contribution is not significant.