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Thioredoxin Reductase Activity may be More Important than GSH Level in Protecting Human Lens Epithelial Cells against UVA Light
Author(s) -
Padgaonkar Vanita A.,
Leverenz Victor R.,
Bhat Aparna V.,
Pelliccia Sara E.,
Giblin Frank J.
Publication year - 2015
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/php.12404
Subject(s) - thioredoxin reductase , glutathione , thioredoxin , buthionine sulfoximine , glutathione reductase , catalase , chemistry , epithelium , biochemistry , antioxidant , dna damage , enzyme , microbiology and biotechnology , biology , dna , glutathione peroxidase , genetics
This study compares the abilities of the glutathione ( GSH ) and thioredoxin (Trx) antioxidant systems in defending cultured human lens epithelial cells ( LEC s) against UVA light. Levels of GSH were depleted with either L‐buthionine‐( S,R )‐sulfoximine ( BSO ) or 1‐chloro‐2,4‐dinitrobenzene ( CDNB ). CDNB treatment also inhibited the activity of thioredoxin reductase (TrxR). Two levels of O 2 , 3% and 20%, were employed during a 1 h exposure of the cells to 25 J cm −2 of UVA radiation (338–400 nm wavelength, peak at 365 nm). Inhibition of TrxR activity by CDNB , combined with exposure to UVA light, produced a substantial loss of LEC s and cell damage, with the effects being considerably more severe at 20% O 2 compared to 3%. In contrast, depletion of GSH by BSO , combined with exposure to UVA light, produced only a slight cell loss, with no apparent morphological effects. Catalase was highly sensitive to UVA ‐induced inactivation, but was not essential for protection. Although UVA light presented a challenge for the lens epithelium, it was well tolerated under normal conditions. The results demonstrate an important role for TrxR activity in defending the lens epithelium against UVA light, possibly related to the ability of the Trx system to assist DNA synthesis following UVA ‐induced cell damage.