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皮肤辐射综合征亚急性期皮肤抗氧化状态的崩溃:一例报告

Collapse of skin antioxidant status during the subacute period of cutaneous radiation syndrome: a case report.

作者信息

Benderitter Marc, Isoir Muriel, Buard Valérie, Durand Valérie, Linard Christine, Vozenin-Brotons Marie Catherine, Steffanazi Jean, Carsin Hervé, Gourmelon Patrick

机构信息

Laboratoire de RadioPathologie, SRBE, DRPH, IRSN, Fontenay-aux Roses, France.

出版信息

Radiat Res. 2007 Jan;167(1):43-50. doi: 10.1667/RR0577.1.

Abstract

This case report describes a patient suffering from accidental cutaneous radiation syndrome. Clinical symptoms were characterized by the presence of moist epidermal denudation over approximately 8% of the body surface without signs of necrosis 88 days after radiation exposure. The skin transcriptional profile was obtained and provides a comprehensive overview of the changes in gene expression associated with skin wound healing after irradiation. In particular, our data show a specific set of genes, i.e. SOD1, GPX1, TDX1, TDX2 and HSP60, implicated in the redox control of normal skin repair after radiation exposure, whereas HOX1 and HOX2 were involved in the pathological skin repair. A reduction in the antioxidant capacity of the irradiated tissue concomitant with a progressive establishment of an uncontrolled inflammatory response was noted. Our data corroborate the hypothesis that ROS modulation is a key element of the healing response after cutaneous exposure to radiation and that the collapse of skin antioxidant status interferes directly with wound healing in skin after radiation exposure. Thus a better understanding of the molecular events through which oxidative stress modulates the healing response could result in a more rational therapeutic approach to the pathological process induced after exposure of skin to radiation.

摘要

本病例报告描述了一名患有意外皮肤辐射综合征的患者。临床症状表现为辐射暴露88天后,体表约8%的皮肤出现湿性表皮剥脱,但无坏死迹象。获取了皮肤转录谱,全面概述了辐射后与皮肤伤口愈合相关的基因表达变化。特别是,我们的数据显示了一组特定的基因,即超氧化物歧化酶1(SOD1)、谷胱甘肽过氧化物酶1(GPX1)、TDX1、TDX2和热休克蛋白60(HSP60),它们参与辐射暴露后正常皮肤修复的氧化还原控制,而HOX1和HOX2则参与病理性皮肤修复。同时注意到,受辐射组织的抗氧化能力下降,伴随着不受控制的炎症反应逐渐形成。我们的数据证实了以下假设:活性氧(ROS)调节是皮肤暴露于辐射后愈合反应的关键因素,皮肤抗氧化状态的崩溃直接干扰辐射后皮肤的伤口愈合。因此,更好地理解氧化应激调节愈合反应的分子事件,可能会为皮肤暴露于辐射后引发的病理过程带来更合理的治疗方法。

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