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Induction of Tumor Necrosis Factor–α by UVB: A Role for Reactive Oxygen Intermediates and Eicosanoids ¶
Author(s) -
Pupe Annemie,
Degreef Hugo,
Garmyn Marjan
Publication year - 2003
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 - 10.1562/0031-8655(2003)0780068iotnfb2.0.co2
Subject(s) - butylated hydroxyanisole , chemistry , nordihydroguaiaretic acid , tumor necrosis factor alpha , reactive oxygen species , lipoxygenase , propyl gallate , cyclooxygenase , pharmacology , phospholipase a2 , biochemistry , arachidonic acid , antioxidant , enzyme , biology , endocrinology
UVB irradiation induces nuclear factor–κB (NF‐κB) activation, tumor necrosis factor–α (TNF‐α) expression and reactive oxygen intermediates (ROI) in keratinocytes. We investigated whether ROI play a role in UVB‐induced TNF‐α mRNA expression. The antioxidants N ‐acetyl cysteine, NAC, epigallocathin gallate, EGCG, butylated hydroxyanisole (BHA) and vitamin C could reduce UVB‐induced TNF‐α mRNA levels to various degrees; vitamin E (α‐tocopherol) had no effect. BHA was the most potent inhibitor. The oxidant tertiary butylated hydroperoxide could effectively induce TNF‐α mRNA expression. Nordihydroguaiaretic acid (NDGA) and MK‐886, inhibitors of lipoxygenase (LOX), and indometacin and quinacrine, inhibitors of cyclooxygenase (COX) and phospholipase A 2 , respectively, could also reduce UVB‐induced TNF‐α mRNA expression. Inhibition by NDGA was in concordance with the results for BHA. NDGA, indometacin, quinacrine and BHA could also effectively inhibit the inhibitor of NF‐κB degradation, thereby maintaining NF‐κB inactivity. In conclusion, we show that ROI are implicated in the induction of TNF‐α mRNA by UVB and that not all antioxidants are equally effective inhibitors. COX products and more importantly LOX products, which themselves are products of an oxidative metabolism, are the main ROI implicated in this induction of TNF‐α expression by UVB probably via activation of NF‐κB.