Suppr超能文献

紫外线照射可能通过抑制金属硫蛋白基因表达来增加培养的人皮肤细胞对镉的敏感性。

Ultraviolet irradiation increases the sensitivity of cultured human skin cells to cadmium probably through the inhibition of metallothionein gene expression.

作者信息

Yamada Hirotomo, Murata Mie, Suzuki Kaoru, Koizumi Shinji

机构信息

Department of Health Effects Research, National Institute of Industrial Health, Tama-ku, Kawasaki 214-8585, Japan.

出版信息

Toxicol Appl Pharmacol. 2004 Nov 1;200(3):251-7. doi: 10.1016/j.taap.2004.04.014.

Abstract

We previously developed an apparatus that can irradiate cultured cells with monochromatic ultraviolet (UV) rays to exactly assess the biological effects of UV components on mammalian cells. Using this device, we studied the effects of UV in and near the UVB region on the general as well as specific protein synthesis of the human skin-derived NB1RGB cells. We found that Cd-induced synthesis of metallothioneins (MTs), which are the proteins involved in the protection against heavy metals and oxidative stress, is inhibited by UV at 280 nm more extensively than total protein synthesis. Such an inhibition was observed when MTs were induced by different inducers such as Cd, Zn, and dexamethasone in three human cell lines, indicating that it is not an event specific to a certain inducer or a certain cell type. By contrast, UV at 300 or 320 nm showed only a marginal effect. UV at 280 nm was likely to block MT gene transcription because Cd-induced increase of MT mRNA was strongly inhibited by irradiation. Cd induction of 70-kDa heat shock protein mRNA was also inhibited by UV irradiation, suggesting that the expression of inducible genes are commonly sensitive to UV. Furthermore, we observed that the irradiation of UV at 280 nm renders NB1RGB cells extremely susceptible to Cd, probably due to the reduced MT synthesis. These observations strongly suggest that UV at 280 nm severely damages cellular inducible protective functions, warning us of a new risk of UV exposure.

摘要

我们之前开发了一种装置,该装置能够用单色紫外线(UV)照射培养的细胞,以准确评估紫外线成分对哺乳动物细胞的生物学效应。利用这一装置,我们研究了UVB区域及其附近的紫外线对人皮肤来源的NB1RGB细胞的一般蛋白质合成以及特定蛋白质合成的影响。我们发现,镉诱导的金属硫蛋白(MTs)的合成受到280nm紫外线的抑制,其程度比总蛋白质合成更广泛,MTs是参与抵御重金属和氧化应激的蛋白质。当在三种人类细胞系中用不同的诱导剂(如镉、锌和地塞米松)诱导MTs时,均观察到这种抑制作用,这表明这并非特定诱导剂或特定细胞类型所特有的现象。相比之下,300或320nm的紫外线仅显示出轻微的影响。280nm的紫外线可能会阻断MT基因转录,因为镉诱导的MT mRNA增加受到照射的强烈抑制。紫外线照射也抑制了镉诱导的70-kDa热休克蛋白mRNA的表达,这表明可诱导基因的表达通常对紫外线敏感。此外,我们观察到,280nm的紫外线照射使NB1RGB细胞对镉极度敏感,这可能是由于MT合成减少所致。这些观察结果强烈表明,280nm的紫外线严重损害细胞的诱导性保护功能,这向我们警示了紫外线暴露的一种新风险。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验