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硒缺乏会使皮肤对紫外线B诱导的氧化损伤和炎症敏感,这涉及p38丝裂原活化蛋白激酶信号通路的激活。

Selenium deficiency sensitizes the skin for UVB-induced oxidative damage and inflammation which involved the activation of p38 MAPK signaling.

作者信息

Zhu Xiaokang, Jiang Mingdong, Song Erqun, Jiang Xiaoji, Song Yang

机构信息

Key Laboratory of Luminescence and Real-Time Analytical Chemistry (Southwest University), Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, China.

Department of Radiation Oncology, The Ninth People's Hospital of Chongqing, Chongqing 400700, China.

出版信息

Food Chem Toxicol. 2015 Jan;75:139-45. doi: 10.1016/j.fct.2014.11.017. Epub 2014 Nov 25.

DOI:10.1016/j.fct.2014.11.017
PMID:25460360
Abstract

Ultraviolet B (UVB) radiation causes oxidative damage and inflammation, and ultimately increases the risk of skin carcinogenesis. Selenium is an essential trace element, previous studies indicated selenium deficiency impairs tissue antioxidant capacity in different experimental models. However, the synergistic effect of selenium deficiency and UVB radiation on skin damage is not clear. In the current study, our data revealed selenium deficiency resulted in further increases of reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS) and phosphorylated H2AX levels, decreases of GSH level and antioxidant enzyme activities in UVB-irradiated mice. Selenium deficiency also exacerbated UVB-induced cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 mRNA expressions. Mechanism studies indicated that UVB-induced p38 signaling was further elevated in the skin of mice maintained with selenium deficiency diet, compared with those maintained with selenium adequate diet. Our investigation suggested that selenium deficiency diet weakens the antioxidant capacity of UVB-irradiated mice skin, which sensitizes to UV radiation-induced oxidative damage and inflammation.

摘要

紫外线B(UVB)辐射会导致氧化损伤和炎症,最终增加皮肤癌发生的风险。硒是一种必需的微量元素,先前的研究表明,在不同的实验模型中,硒缺乏会损害组织的抗氧化能力。然而,硒缺乏与UVB辐射对皮肤损伤的协同作用尚不清楚。在当前的研究中,我们的数据显示,硒缺乏导致UVB照射小鼠体内活性氧(ROS)、硫代巴比妥酸反应性物质(TBARS)和磷酸化H2AX水平进一步升高,谷胱甘肽(GSH)水平和抗氧化酶活性降低。硒缺乏还加剧了UVB诱导的环氧合酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和IL-6 mRNA表达。机制研究表明,与给予充足硒饮食的小鼠相比,给予缺硒饮食的小鼠皮肤中,UVB诱导的p38信号进一步增强。我们的研究表明,缺硒饮食会削弱UVB照射小鼠皮肤的抗氧化能力,使其对UV辐射诱导的氧化损伤和炎症更加敏感。

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