Cancer Institute, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China.
The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China.
Clin Exp Dermatol. 2019 Jul;44(5):512-519. doi: 10.1111/ced.13834. Epub 2018 Nov 19.
Ultraviolet (UV)B radiation has long been considered a carcinogen in both epidemiological surveys and experimental studies. However, recent work has suggested that different dosages of UVB exert different influences on cells. There are also co-carcinogenesis factors such as arsenic that affect the role of UVB.
To explore the co-carcinogenesis effect of UVB and arsenic on the mouse epidermal cell line JB6 and the mechanism underlying it.
Growth of JB6 cells was measured by MTT assay. We carried out a comet assay to determine the DNA damage caused by UVB and arsenic, and tested the expression of DNA repair protein by western blotting. Reactive oxygen species (ROS) were measured using DCF and DHE staining, and changes in antioxidant enzymes were assessed using western blotting.
Viability assays showed that arsenic increased the UVB-induced death rate. Arsenic enhanced DNA damage caused by UVB both directly by injury to double-stranded DNA and indirectly by reducing the capability of DNA repair in JB6 cells. All of these effects are the results of increased ROS generation and reduced expression of the antioxidant enzyme superoxide dismutase (SOD)1.
Arsenic was found to enhance UVB-induced production of ROS and to downregulate SOD1 expression, leading to DNA damage and apoptosis in mouse skin cells. The combination of arsenic and UVB exposure was found to differentially regulate the expression of SOD1 and SOD2.
紫外线（UV）B 辐射一直被认为是流行病学调查和实验研究中的致癌因素。然而，最近的研究表明，不同剂量的 UVB 对细胞有不同的影响。还有砷等协同致癌因素会影响 UVB 的作用。
探讨 UVB 和砷对小鼠表皮细胞系 JB6 的协同致癌作用及其机制。
通过 MTT 法测定 JB6 细胞的生长情况。我们进行彗星试验以确定 UVB 和砷引起的 DNA 损伤，并通过 Western blot 检测 DNA 修复蛋白的表达。使用 DCF 和 DHE 染色测定活性氧（ROS），通过 Western blot 评估抗氧化酶的变化。
细胞活力测定表明，砷增加了 UVB 诱导的死亡率。砷直接通过损伤双链 DNA 以及间接通过降低 JB6 细胞的 DNA 修复能力增强了 UVB 引起的 DNA 损伤。所有这些作用都是由于 ROS 生成增加和抗氧化酶超氧化物歧化酶 1（SOD1）表达减少所致。
发现砷增强了 UVB 诱导的 ROS 生成，并下调了 SOD1 表达，导致小鼠皮肤细胞的 DNA 损伤和凋亡。砷和 UVB 暴露的联合作用发现会差异调节 SOD1 和 SOD2 的表达。
