Obesity increases the risk of UV radiation-induced oxidative stress and activation of MAPK and NF-κB signaling

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• 作者：Santosh K. Katiyar ; Syed M. Meeran
• 关键词：Skin ; Oxidative stress ; Hydrogen peroxide ; Glutathione peroxidase ; Mitogen-activated protein kinase ; NF-κ ; B ; Cytokines ; Ultraviolet radiation ; Free radicals
• 刊名：Free Radical Biology and Medicine
• 出版年：2007
• 期刊代码：105_08915849
• 类别：med
• 出版时间：15 January 2007
• 卷：42
• 期：2
• 页码：299-310
• 文件大小：1057 K

摘要

Obesity has been implicated in several diseases, including cancer; however, the relationship of obesity and susceptibility to ultraviolet (UV) radiation-caused skin diseases has not been investigated. As UV-induced oxidative stress has been implicated in several skin diseases, we assessed the role of obesity on UVB-induced oxidative stress in genetically obese Lep^ob/Lep^ob (leptin-deficient) mice. Here, we report that chronic exposure to UVB (120 mJ/cm²) resulted in greater oxidative stress in the skin of obese mice in terms of higher levels of H₂O₂ and NO production, photo-oxidative damage of lipids and proteins, and greater depletion of antioxidant defense enzymes, like glutathione, glutathione peroxidase, and catalase. As UV-induced oxidative stress mediates activation of MAPK and NF-κB signaling pathways, we determined the effects of UVB on these pathways in obese mice. Exposure of obese mice to UVB resulted in phosphorylation of ERK1/2, JNK, and p38 proteins of the MAPK family. Compared to wild-type mice, the obese mice exhibited higher levels of phosphorylation of these proteins, greater activation of NF-κB/p65, and higher levels of circulating proinflammatory cytokines, including TNF-α, IL-1β and IL-6, on UVB irradiation. Taking these results together, our study suggests for the first time that obesity in mice is associated with greater susceptibility to UVB-induced oxidative stress and therefore may be a risk factor for skin diseases associated with UVB-induced oxidative stress.