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红外辐射 A 的预辐照增强了紫外线 B 诱导的细胞凋亡并消除了 DNA 损伤,但不依赖于 DNA 损伤修复。

Enhancement of Ultraviolet B-Induced Apoptosis and Elimination of DNA Damage by Pre-Irradiation with Infrared Radiation A Does Not Depend on DNA Damage Repair.

机构信息

Department of Dermatology, Nippon Medical School.

出版信息

J Nippon Med Sch. 2022 May 12;89(2):184-189. doi: 10.1272/jnms.JNMS.2022_89-213. Epub 2021 Sep 14.

Abstract

BACKGROUND

We previously reported that pre-irradiation with infrared radiation A (IRA) eliminated ultraviolet B (UVB) -induced cyclobutane pyrimidine dimers (CPDs). Accelerated elimination of CPDs could have resulted from enhanced DNA repair and/or enhanced induction of apoptosis. Using Xpa knockout (KO) mice, which are deficient in DNA repair, we examined whether IRA accelerated elimination of CPDs by enhancing DNA repair.

METHODS

We have already generated mice harboring epidermal melanocytes that produce only eumelanin and dominant pheomelanin, and no melanin. To obtain such mice with impaired DNA repair ability, we backcrossed them with Xpa KO mice. Three hours before UVB irradiation, the mice were irradiated with IRA, and CPDs and apoptotic cells were examined.

RESULTS

Pre-irradiation of Xpa KO mice with IRA before UVB irradiation accelerated removal of CPDs and enhanced apoptotic changes.

CONCLUSION

These results indicate that enhancement of UVB-induced apoptosis and acceleration of removal of CPDs by pre-irradiation with IRA does not depend on DNA damage repair.

摘要

背景

我们之前曾报道过,红外辐射 A(IRA)的预辐照可消除紫外线 B(UVB)诱导的环丁烷嘧啶二聚体(CPD)。CPD 的加速消除可能是由于增强的 DNA 修复和/或增强的细胞凋亡诱导所致。利用 Xpa 敲除(KO)小鼠,其 DNA 修复能力缺失,我们研究了 IRA 是否通过增强 DNA 修复来加速 CPD 的消除。

方法

我们已经培育出了仅产生真黑色素和显性棕黑色素、而不产生黑色素的表皮黑素细胞的小鼠。为了获得这种 DNA 修复能力受损的小鼠,我们将其与 Xpa KO 小鼠进行了回交。在 UVB 照射前 3 小时,用 IRA 照射小鼠,然后检查 CPD 和凋亡细胞。

结果

在 UVB 照射前,用 IRA 对 Xpa KO 小鼠进行预辐照可加速 CPD 的清除并增强凋亡变化。

结论

这些结果表明,IRA 预辐照增强 UVB 诱导的细胞凋亡和加速 CPD 清除并不依赖于 DNA 损伤修复。

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