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UVB irradiation-induced impairment of keratinocytes and adaptive responses to oxidative stress.

机译:UVB辐射诱导的角质形成细胞损伤和对氧化应激的适应性反应。

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UVB irradiation of human skin is known to induce pathophysiological processes as oxidative stress and inflammation. HaCaT keratinocytes represent a well-established in vitro model system to investigate the influence of UVB irradiation on cell cultures. It was the aim of these investigations to study the effects of moderate UVB doses on cellular and mitochondrial integrity of HaCaT keratinocytes, biomarkers of oxidative stress and antioxidant protection by superoxide dismutases. F(2)-isoprostane concentrations were UVB dose-dependently enhanced reaching a plateau at 50 mJ/cm(2). Cell viability was reduced and apoptosis was enhanced with increasing UVB doses. The activities of the respiratory chain complexes were practically not altered at lower UVB doses, up to 50 mJ/cm(2), whereas remarkable decreases, also for the levels of cardiolipin species, were seen at 100 mJ/cm(2). As an adaptive response to the enhanced oxidative stress, protein levels of MnSOD increased about 3-fold at 50 mJ/cm(2) and decreased at higher doses. From the data it can be concluded that keratinocytes are sufficiently protected at low UVB doses, whereas higher doses lead to irreversible cell damage.
机译:已知人类皮肤的UVB辐射会诱发诸如氧化应激和炎症的病理生理过程。 HaCaT角质形成细胞代表一个完善的体外模型系统,以研究UVB辐射对细胞培养物的影响。这些研究的目的是研究中等剂量的UVB对HaCaT角质形成细胞的细胞和线粒体完整性,氧化应激的生物标记和超氧化物歧化酶的抗氧化保护的影响。 F(2)-异前列腺素浓度是UVB剂量依赖性增强的,在50 mJ / cm(2)时达到稳定水平。随着UVB剂量的增加,细胞活力降低,凋亡增强。在较低的UVB剂量下,高达50 mJ / cm(2),呼吸链复合物的活性几乎没有改变,而在100 mJ / cm(2)下,心磷脂种类的水平也出现了明显的下降。作为对增强的氧化应激的适应性反应,MnSOD的蛋白质水平在50 mJ / cm(2)时增加约3倍,而在更高剂量时降低。从数据可以得出结论,在低UVB剂量下角质形成细胞得到了充分的保护,而较高剂量则导致不可逆的细胞损伤。

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