Naderi-Hachtroudi Lale, Peters Thorsten, Brenneisen Peter, Meewes Christian, Hommel Christina, Razi-Wolf Ziba, Schneider Lars A, Schüller Jutta, Wlaschek Meinhard, Scharffetter-Kochanek Karin
Department of Dermatology, University of Cologne, Germany.
Arch Dermatol. 2002 Nov;138(11):1473-9. doi: 10.1001/archderm.138.11.1473.
Reactive oxygen species generated in the skin by UV irradiation promote photoaging and photocarcinogenesis. The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation.
To determine whether repetitive UV-B exposure, as practiced for light hardening during phototherapy for various photodermatoses, can enhance the adaptive antioxidant response by up-regulating MnSOD activity in either the epidermal or the dermal skin compartment.
In vitro experiments to determine MnSOD activity levels in cultured human dermal fibroblasts and epidermal cells (HaCaT cells and primary keratinocytes) at different times after direct UV-B exposure or after incubation of human dermal fibroblasts with supernatants from UV-B-irradiated epidermal cells.
Photobiological research laboratory in a university dermatology department.
Irradiation of cultured human dermal fibroblasts and epidermal cells with UV-B.
Manganese SOD messenger RNA and activity levels in cultured irradiated or mock-treated skin cells.
No increase in MnSOD activity could be detected in fibroblasts or epidermal cells until 24 hours after UV-B irradiation. However, fibroblasts incubated with supernatants from UV-B-irradiated epidermal cells showed a marked increase in specific MnSOD messenger RNA and activity. Removal of interleukin 1alpha, interleukin 1beta, and tumor necrosis factor alpha from the supernatants led to a significant reduction of MnSOD mRNA in fibroblasts.
Irradiation of the epidermal cells with UV-B induced a release of soluble factors that amplified MnSOD activity in fibroblasts via a paracrine mechanism.
紫外线照射在皮肤中产生的活性氧会促进光老化和光致癌作用。锰（Mn）超氧化物歧化酶（SOD）是一种主要的抗氧化酶，对线粒体内氧自由基的稳态起着关键作用，因此在衰老和肿瘤发生的控制中起着至关重要的作用。
确定在各种光皮肤病的光疗过程中用于光硬化的重复紫外线B照射是否能通过上调表皮或真皮皮肤层中的MnSOD活性来增强适应性抗氧化反应。
体外实验，以确定在直接紫外线B照射后不同时间或用人皮肤成纤维细胞与紫外线B照射的表皮细胞的上清液孵育后，培养的人皮肤成纤维细胞和表皮细胞（HaCaT细胞和原代角质形成细胞）中的MnSOD活性水平。
一所大学皮肤科的光生物学研究实验室。
用紫外线B照射培养的人皮肤成纤维细胞和表皮细胞。
培养的照射或模拟处理的皮肤细胞中锰超氧化物歧化酶信使核糖核酸和活性水平。
在紫外线B照射后24小时之前，未在成纤维细胞或表皮细胞中检测到MnSOD活性增加。然而，用人皮肤成纤维细胞与紫外线B照射的表皮细胞的上清液孵育后，其特异性MnSOD信使核糖核酸和活性显著增加。从上清液中去除白细胞介素1α、白细胞介素1β和肿瘤坏死因子α导致成纤维细胞中MnSOD mRNA显著减少。
紫外线B照射表皮细胞可诱导可溶性因子释放，这些因子通过旁分泌机制放大成纤维细胞中的MnSOD活性。
