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氧化应激、氧化还原与肿瘤微环境

Oxidative stress, redox, and the tumor microenvironment.

作者信息

Cook John A, Gius David, Wink David A, Krishna Murali C, Russo Angelo, Mitchell James B

机构信息

Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.

出版信息

Semin Radiat Oncol. 2004 Jul;14(3):259-66. doi: 10.1016/j.semradonc.2004.04.001.

Abstract

Cellular metabolism is critical for the generation of energy in biological systems; however, as a result of electron transfer reactions, reactive oxygen species (ROS) are generated in aerobic cells. Although low amounts of ROS are easily tolerated by the cell, abnormally high levels of ROS induce oxidative stress. ROS are also produced after exposure to ionizing radiation, selected chemotherapeutic agents, hyperthermia, inhibition of antioxidant enzymes, or depletion of cellular reductants such as NADPH and glutathione. Oxidative stress such as ionizing radiation produces a variety of highly reactive free radicals that damage cells, initiate signal transduction pathways, and alter gene expression. Cells are capable of countering the effects of oxidative stress by virtue of a complex redox buffering system. With respect to the radiation treatment of cancer, components of the cellular redox armamentarium may be targeted to enhance cell killing in the case of tumors and/or protection in the case of normal tissues.

摘要

细胞代谢对于生物系统中能量的产生至关重要;然而,由于电子转移反应,需氧细胞中会产生活性氧(ROS)。虽然细胞能够轻松耐受少量的ROS,但异常高水平的ROS会诱导氧化应激。暴露于电离辐射、某些化疗药物、热疗、抗氧化酶抑制或细胞还原剂(如NADPH和谷胱甘肽)耗竭后也会产生活性氧。诸如电离辐射等氧化应激会产生多种高反应性自由基,这些自由基会损伤细胞、启动信号转导通路并改变基因表达。细胞能够借助复杂的氧化还原缓冲系统对抗氧化应激的影响。就癌症的放射治疗而言,细胞氧化还原防御机制的组成部分可作为靶点,在肿瘤治疗中增强细胞杀伤作用和/或在正常组织治疗中起到保护作用。

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