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Role of Hydrogen Peroxide in the Cytotoxic Effects of UVA/B Radiation on Mammalian Cells
Author(s) -
Bertling Chad J.,
Lin Fubao,
Girotti Albert W.
Publication year - 1996
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.1751-1097.1996.tb02433.x
Subject(s) - cytotoxic t cell , hydrogen peroxide , chemistry , l1210 cells , microbiology and biotechnology , photosensitivity , catalase , glutathione peroxidase , selenium , glutathione , cell culture , peroxidase , cytotoxicity , stereochemistry , enzyme , biochemistry , biology , in vitro , physics , genetics , quantum mechanics , organic chemistry
Effects of selenium (Se) deficiency on the sensitivity of murine leukemia L1210 cells to broad band UVA/B radiation (310–400nm) have been investigated. Cells rendered glutathione peroxidase (GPX) deficient by shortterm (2–3week) growth in 1% serum/RPMI medium without added Se [LSe(‐) cells] were found to be much less resistant to clonally assessed UVA/B lethality than Se‐supplemented controls [LSe(+) cells]. By contrast, long‐term (>20 week) Se‐deprived [L'Se(‐)] cells whose catalase (CAT) activity was elevated >100‐fold were far more resistant to UVA/B than LSe(+) cells. Similar trends were observed for cells irradiated in 1% serum/RPMI or Hank's medium. Whereas the CAT inhibitor 3‐amino‐1,2,4‐triazole had no effect on LSe(+) photosensitivity, it produced a large increase in L' Se(‐) photosensitivity. These findings are consistent with H 2 O 2 in‐termediacy in photokilling and suggest that L1210 cells depend mainly on GPX for protection against this species but switch to overexpressed CAT after chronic Se deprivation. In agreement with this, steady‐state H 2 O 2 levels measured by H 2 O 2 electrode during UVA/B exposure were higher in LSe(‐) than LSe(+) suspensions but much lower (barely detectable) in L' Se(‐) suspensions. Cytotoxic effects of UVA/B and variations thereof resulting from Se manipulation could be mimicked by treating cells with glucose oxidase in the presence of D‐glucose, providing further support for H 2 O 2 involvement. Whether UVA/B‐generated H 2 O 2 is directly cytotoxic or gives rise to a more damaging species such as hydroxyl radical (HO) is presently unknown.