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Protection against ultraviolet A‐induced oxidative damage in normal human epidermal keratinocytes under post‐menopausal conditions by an ultraviolet A‐activated caged‐iron chelator: a pilot study
Author(s) -
Pelle Edward,
Jian Jinlong,
Declercq Lieve,
Dong Kelly,
Yang Qing,
Pourzand Charareh,
Maes Daniel,
Pernodet Nadine,
Yarosh Daniel B.,
Huang Xi
Publication year - 2011
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/j.1600-0781.2011.00604.x
Subject(s) - oxidative stress , chemistry , lipid peroxidation , ferritin , reactive oxygen species , biochemistry , human skin , biology , genetics
Background/purpose: Human skin is constantly exposed to ultraviolet A (UVA), which can generate reactive oxygen species and cause iron release from ferritin, leading to oxidative damage in biomolecules. This is particularly true in post‐menopausal skin due to an increase in iron as a result of menopause. As iron is generally released through desquamation, the skin becomes a main portal for the release of excess iron in this age group. In the present study, we examined a strategy for controlling UVA‐ and iron‐induced oxidative stress in skin using a keratinocyte post‐menopausal cellular model system. Methods: Keratinocytes that had been cultured under normal or high‐iron, low‐estrogen conditions were treated with (2‐nitrophenyl) ethyl pyridoxal isonicotinoyl hydrazone (2‐PNE‐PIH). 2‐PNE‐PIH is a caged‐iron chelator that does not normally bind iron but can be activated by UVA radiation to bind iron. Following incubation with 2‐PNE‐PIH, the cells were exposed to 5 J/cm 2 UVA and then measured for changes in lipid peroxidation and ferritin levels. Results: 2‐PNE‐PIH protected keratinocytes against UVA‐induced lipid peroxidation and ferritin depletion. Further, 2‐PNE‐PIH was neither cytotoxic nor did it alter iron metabolism. Conclusion: 2‐PNE‐PIH may be a useful deterrent against UVA‐induced oxidative stress in post‐menopausal women.