辐射防护 ›› 2022, Vol. 42 ›› Issue (2): 111-118.
蔡卫超, 曹卫红
收稿日期:
2021-01-18
出版日期:
2022-03-20
发布日期:
2022-04-29
通讯作者:
曹卫红。E-mail: caoweihong@hotmail.com
作者简介:
蔡卫超(1994—),男,2012年9月至2019年6月苏州大学临床医学(本硕连读)专业,硕士,医师。E-mail:690029840@qq.com
CAI Weichao, CAO Weihong
Received:
2021-01-18
Online:
2022-03-20
Published:
2022-04-29
摘要: 机体受到意外照射或在接受放射治疗时会引起放射性皮肤损伤,皮肤组织中最先发生水分解而产生活性氧,其次呼吸链及炎症过程也会产生大量活性氧。活性氧作为信号分子在调控生理生化过程中起到了不可替代的作用。本文就辐射刺激后皮肤内活性氧变化、活性氧干预放射性皮肤损伤的机制以及活性氧消除调控放射性损伤等三个方面的研究进展进行综述,旨在联系活性氧代谢与放射性损伤的生理病理反应,为相关研究及临床治疗提供便利。
中图分类号:
蔡卫超, 曹卫红. 活性氧与放射性皮肤损伤的研究进展[J]. 辐射防护, 2022, 42(2): 111-118.
CAI Weichao, CAO Weihong. Research progress of reactive oxygen species and radiation-induced skin injury[J]. RADIATION PROTECTION, 2022, 42(2): 111-118.
[1] Axent M, He J, Bass C P. An alternative approach to histopath logical validation of PET imaging for radiation therapy image guidance: a proof of concept[J]. Radiother 0ncol, 2014, 110(2): 309-316. [2] Jaworowski Z. Observations on the Chernobyl Disaster and LNT[J]. Dose Response, 2010, 8(2):148-171. [3] ZHU Y, BU Q, LIU X, et al. Neuroprotective effect of TAT-14-3-3 fusion protein against cerebral ischemia reperfusion injury in rats[J]. PLos One, 2014, 9(3): 933-934. [4] Kim J H, Kolozsvary A J, Jenrow K A, et al. Mechanisms of radiation-induced skin injury and implications for future clinical trials[J]. Int J Radiat Biol, 2013, 89(5):311-318. [5] Jakubczyk K, Dec K, Kałduńska J, et al. Reactive oxygen species-sources, functions, oxidative damage[J]. Pol Merkur Lekarski, 2020, 48(284): 124-127. [6] Husain K, Hernandez W, Ansari R A, et al. Inflammation, oxidative stress and renin angiotensin system in atherosclerosis[J]. World J Biol Chem, 2015, 6(3): 209-217. [7] De Grey A D. Reactive oxygen species production in the mitochondrial matrix: implications for the mechanism of mitochondrial mutation accumulation[J]. Rejuvenation Res, 2005, 8(1): 13-17. [8] Benmoussa K, Authier H, Prat M, et al. P17, an original host defense peptide from ant venom, promotes antifungal activities of macrophages through the induction of C-type lectin receptors dependent on LTB4-mediated PPAR γ activation[J]. Front Immunol, 2017, 8: 1650. [9] XUE J, YU C, SHENG W, et al. The Nrf2/GCH1/BH4 Axis ameliorates radiation-induced skin injury by modulating the ROS cascade[J]. Invest Dermatol, 2017, 137(10): 2059-2068. [10] Zucker S N, Fink E E, Bagati A, et al. Nrf2 amplifies oxidative stress via induction of Klf9[J]. Mol Cell, 2014, 53(6): 916-928. [11] Parsons M J, Green D R. Mitochondria in cell death[J]. Essays Biochem, 2010, 47: 99-114. [12] ZHANG Q, DENG Y, LAi W, et al. Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation[J]. Sci Rep, 2016, 6: 30146. [13] SHI M, HUANG J, SUN X, et al. Effect of rivaroxaban on the injury during endotoxin-induced damage to human umbilical vein endothelial cells[J]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue, 2019, 31(4): 468-473. [14] Hassan W, Ding L, Gao R Y, et al. Interleukin-6 signal transduction and its role in hepatic lipid metabolic disorders[J]. Cytokine, 2014, 66(2): 133-142. [15] Schreck I, Alrawi M, Mingot J M, et al. C-jun localizes to the nucleus independent of its phosphorylation by and interaction with JNK and vice versa promotes nuclear accumulation of JNK[J]. Biochem Biophys Res Commun, 2011, 407(4): 735-740. [16] Li G B, LIU J Y, FENG X M, et al. Retigabine attenuates focal cerebral ischemic injury through inhibiting mitochondria-dependent apoptotic pathway[J]. Eur Rev Med Pharmacol Sci, 2018, 22(15): 5018-5023. [17] HAN A, ZOU L, GAN X, et al. ROS generation and MAPKs activation contribute to the Ni-induced testosterone synthesis disturbance in rat Leydig cells[J]. Toxicol Lett, 2018, 290: 36-45. [18] Kapoor M, Sharma N, Sandhir R, et al. Effect of the NADPH oxidase inhibitor apocynin on ischemia-reperfusion hippocampus injury in rat brain[J]. Biomed Pharmacother, 2018, (97): 458-472. [19] Fulda S, Gorman A M, Hori O, et al. Cellular stress responses: cell survival and cell death[J]. Int J Cell Biol, 2010, 2010: 214074. [20] Gorbunov N V, Kiang J G. Up-regulation of autophagy in small intestine Paneth cells in response to total-body gamma-irradiation[J]. J Pathol, 2009, 219(2): 242-252. [21] YUAN G J, DENG J J, CAO D D, et al. Autophagic cell death induced by reactive oxygen species is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells[J]. World J Gastroenterol, 2017, 23(30): 5530-5537. [22] WANG C, LI T K, ZENG C H, et al. Iodine-125 seed radiation induces ROS-mediated apoptosis, autophagy and paraptosis in human esophageal squamous cell carcinoma cells[J]. Oncol Rep, 2020, 43: 2028-2044. [23] Lin J H, Walter P, Yen T S. Endoplasmic reticulum stress in disease pathogenesis[J]. Annu Rev Pathol, 2008, 3: 399-425. [24] Kumar P, Raman T, Swain M M, et al. Hyperglycemia-Induced oxidative-nitrosative stress induces inflammation and neurodegeneration via augmented tuberous sclerosis complex-2 (TSC-2) activation in neuronal cells[J]. Mol Neurobiol, 2017, 54(1): 238-254. [25] Cárdenas C, Foskett J K. Mitochondrial Ca(2+) signals in autophagy[J]. Cell Calcium, 2012, 52(1): 44-51. [26] Pfisterer S G, Mauthe M. Ca2+/calmodulin-dependent kinase (CaMK) signaling via CaMKI and AMP-activated protein kinase contributes to the regulation of WIPI-1 at the onset of autophagy[J]. Mol Pharmacol, 2011, 80(6): 1066-1075. [27] Pankiv S, Lamark T, Bruun J A, et al. Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies[J]. X J Biol Chem, 2010, 285(8): 5941-5953. [28] Guven M, Brem R, Macpherson P, et al. Oxidative damage to RPA Limits the nucleotide excision repair capacity of human cells[J]. J Invest Dermatol, 2015, 135(11): 2834-2841. [29] Czarny P, Pawlowska E, Bialkowska-Warzecha J, et al. Autophagy in DNA damage response[J]. Int J Mol Sci, 2015, 16(2): 2641-2662. [30] Chaurasia M, Bhatt A N, Das A, et al. Radiation-induced autophagy: mechanisms and consequences[J]. Free Radic Res, 2016, 50(3): 273-290. [31] Sies H. Hydrogen peroxide as a central redox signalingmolecule in physiological oxidative stress: Oxidative eustress[J]. Redox Biol, 2017, 11: 613-619. [32] 凤琦, 张晶钰. ROS与过氧化氢的研究现状及新进展[J]. 基因组学与应用生物学, 2020, 39(2): 726-731. FENG Q, ZHANG J Y. Research status and new progress on ROS and hydrogen peroxide[J]. Genomics and Applied Biology, 2020, 39 (2): 726-731. [33] WAN S, JIANG L. Erratum to: Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in plants[J]. Protoplasma, 2016, 253(3): 765. [34] Bhandary B, Marahatta A, Kim H R, et al. An involve-ment of oxidative stress in endoplasmic reticulumstress and its associated diseases[J]. Int J Mol Sci, 2012, 14: 434-456. [35] Diehn M, Cho R W, Lobo N A, et al. Association of reactive oxygen species levels and radioresistance in cancer stem cells[J]. Nature, 2009, 458(7239): 780-783. [36] Manda K, Kavanagh J N, Buttler D, et al. Low dose effects of ionizing radiation on normal tissue stem cells[J]. Mutat Res Rev Mutat Res, 2014, 02.003. [37] Pazzaglia S, Briganti G, Mancuso M, et al. Neurocognitive decline following radiotherapy: mechanisms and therapeutic implications[J]. Cancers (Basel) , 2020, 12(1): 146-159. [38] HUANG B, HE T, YAO Q, et al. Amifostine suppresses the side effects of radiation on BMSCs by promoting cell proliferation and reducing ROS production[J]. Stem Cells Int, 2019, 2019: 8749090. [39] Kumar S, Suman S, Fornace A J, et al. Intestinal stem cells acquire premature senescence and senescence associated secretory phenotype concurrent with persistent DNA damage after heavy ion radiation in mice[J]. Aging (Albany NY), 2019, 11(12): 4145-4158. [40] Rodrigues-Moreira S, Moreno S G, Ghinatti G, et al. Low-dose irradiation promotes persistent oxidative stress and decreases self-renewal in hematopoietic stem cells[J]. Cell Rep, 2017, 20(13): 3199-3211. [41] Ahmad I M, Abdalla M Y, Moore T A, et al. Healthcare workers occupationally exposed to ionizing radiation exhibit altered levels of inflammatory cytokines and redox parameters[J]. Antioxidants (Basel), 2019 8(1): 12-25. [42] SU L, WANG Z, HUANG F, et al. 18β-Glycyrrhetinic acid mitigates radiation-induced skin damage via NADPH oxidase/ROS/p38MAPK and NF-κB pathways[J]. Environ Toxicol Pharmacol, 2018, 60: 82-90. [43] WANG Y, XU X, ZHAO P, et al. Escin Ia suppresses the metastasis of triple-negative breast cancer by inhibiting epithelial-mesenchymal transition via down-regulating LOXL2 expression[J]. Oncotarget, 2016, 7(17): 23684-23699. [44] Carrillo-Gálvez A B, Gálvez-Peisl S, González-Correa J E, et al. GARP is a key molecule for mesenchymal stromal cell responses to TGF-β and fundamental to control mitochondrial ROS levels[J]. Stem Cells Transl Med, 2020, 9(5): 636-650. [45] Fazzi F, Njah J, Di Giuseppe M, et al. TNFR1/phox interaction and TNFR1 mitochondrial translocation Thwart silica-indu.ced pulmonary fibrosis[J]. J Immunol, 2014, 192(8): 3837-3846. [46] PEI H, ZHANG J, NIE J, et al. RAC2-P38 MAPK-dependent NADPH oxidase activity is associated with the resistance of quiescent cells to ionizing radiation[J]. Cell Cycle, 2017, 16(1): 113-122. [47] Kim J H, Kolozsvary A J, Jenrow K A, et al. Mechanisms of radiation-induced skin injury and implications for future clinical trials[J]. Int J Radiat Biol, 2013, 89(5): 311-318. [48] DI A, GAO X P, QIAN F, et al. The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation[J]. Nat Immunol, 2011, 13(1): 29-34. [49] CHEN C C, CHENG Y Y. Cyclooxygenase-2 expression is up-regulated by 2-aminobiphenyl in a ROS and MAPK-dependent signaling pathway in a bladder cancer cell line[J]. Chem Res Toxicol, 2012, 25(3): 695-705. [50] WU Q, Allouch A, Paoletti A, et al. NOX2-dependent ATM kinase activation dictates pro-inflammatory macrophage phenotype and improves effectiveness to radiation therapy[J]. Cell Death Differ, 2017, 24(9): 1632-1644. [51] 龚玉华, 徐中叶. 放射诱导旁观者效应的研究进展[J]. 医疗装备, 2019, 32(1): 201-203. GONG Y H, XU Z Y. Research progress of radiation-induced bystander effect[J]. Chinese Journal Medical Device, 2019, 32 (1): 201-203. [52] DONG C, TU W, HE M, et al. Role of endoplasmic reticulum and mitochondrion in proton microbeam radiation-induced bystander effect[J]. Radiat Res, 2020, 193(1): 63-72. [53] Genro Kashino, Yuki Tamari, Jun Kumagai, et al. Suppressive effect of ascorbic acid on the mutagenesis induced by the bystander effect through mitochondrial function[J]. Free Radic Res, 2013, 47(6-7): 474-479. [54] XU W, WANG T, XU S, et al. Radiation-induced epigenetic bystander effects demonstrated in Arabidopsis thaliana[J]. Radiat Res, 2015, 183(5): 511-524. [55] 邹佳, 宋海峰. 抗氧化物在辐射损伤防治研究中的新进展[J]. 辐射研究与辐射工艺学报, 2012, 30(3): 142-147. ZOU J, SONG H F. New progress of antioxidants in the prevention and treatment of radiation damage[J]. Journal of Radiation Research and Radiation Processing, 2012, 30 (3): 142-147. [56] Formentini L, Santacatterina F. Mitochondrial ROS production protects the intestine from inflammation through functional M2 macrophage polarization[J]. Cell Rep, 2017, 19(6): 1202-1213. [57] YAO J, CHENG Y, ZHOU M, et al. ROS scavenging MnO nanozymes for anti-inflammation[J]. Chem Sci, 2018, 9(11): 2927-2933. [58] ZHANG Y R, WANG J Y. Design and synthesis a mitochondria-targeted dihydronicotinamide as radioprotector[J]. Free Radic Biol Med, 2019, 136: 45-51. [59] Gudkov S V, Guryev E L, Gapeyev A B, et al. Unmodified hydrated С fullerene molecules exhibit antioxidant properties, prevent damage to DNA and proteins induced by reactive oxygen species and protect mice against injuries caused by radiation-induced oxidative stress[J]. Nanomedicine, 2019, 15(1): 37-46. [60] ZHANG Y R, LI Y Y, WANG J Y, et al. Synthesis and characterization of a rosmarinic acid derivative that targets mitochondria and protects against radiation-induced damage in vitro[J]. Radiat Res, 2017, 188(3) : 264-275. [61] LI M, LANG Y, GU M M, et al. Vanillin derivative VND3207 activates DNA-PKcs conferring protection against radiation-induced intestinal epithelial cells injury in vitro and in vivo[J]. Toxicol Appl Pharmacol, 2020, 387: 114855. |
[1] | 朱梦梅, 欧阳涛, 华天桢, 李琨, 于兵. 胞外超氧化物歧化酶(EC-SOD)抗辐射作用的研究进展[J]. 辐射防护, 2022, 42(2): 102-110. |
[2] | 黄越, 陈乃耀, 赵辉, 闫振宇, 张海霞, 赵雪聪, 张丁平. N-乙酰半胱氨酸对HT22细胞辐射诱导氧化应激及增殖和凋亡的影响[J]. 辐射防护, 2021, 41(2): 165-173. |
[3] | 上伟, 王守正, 张惠生, 李丽, 凌燕, 杜治国, 温文, 卢耻桥. 2003—2018年我院处置的辐射事故病例分析[J]. 辐射防护, 2021, 41(1): 76-80. |
[4] | 王优优, 刘玉龙, 余道江, 卞华慧, 陈炜博, 戴宏, 冯骏超, 侯雨含, 于军. 一例手指急性放射性皮肤损伤患者的诊治和医学随访[J]. 辐射防护, 2019, 39(6): 528-531. |
[5] | 王锃, 洪金省, 陈金梅, 吴建东, 苏丽. 淫羊藿素对人角质形成细胞HaCat辐射损伤的保护作用[J]. 辐射防护, 2019, 39(4): 338-344. |
[6] | 胡雅梦, 龙颖, 陈科良, 刘奔波, 何淑雅, 黄波. 黄芪甲苷对肝细胞放射损伤预防作用的机制研究[J]. 辐射防护, 2017, 37(4): 309-316. |
[7] | 李超, 李忠秋, 李雪萍, 杨洋, 曾妍, 潘秀颉, 杨陟华, 朱茂祥, 顾永清. 盐诱导激酶2对电离辐射诱导的自噬与凋亡的影响[J]. 辐射防护, 2017, 37(3): 214-222. |
[8] | 李文波, 庞华, 周静, 吴宏, 姜蓉. 枸杞多糖对受X射线照射小鼠外周血象及骨髓单个核细胞的影响[J]. 辐射防护, 2016, 36(4): 218-223. |
|