Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses.
Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses.
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DOI：
10.3390/antiox6040075
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发表时间：
2017-09-28
期刊：
影响因子：
--
通讯作者：
St Clair DK
中科院分区：
文献类型：
--
作者：
Yarana C;St Clair DK
化疗的短期和长期副作用限制了最大治疗剂量，并损害了幸存者的生活质量。对正常组织的损伤，特别是化疗引起的心肌病，是一种意想不到的结果，会对健康造成破坏性影响。美国食品和药物管理局批准用于癌症治疗的药物中约有一半与活性氧的产生有关，阿霉素（Dox）就是其中之一。Dox通过使其醌结构参与超氧化物自由基的产生而经历氧化还原循环，这被认为有助于其在心肌病中发挥作用。Dox诱导的蛋白质氧化改变了对细胞有毒的蛋白质功能、易位和聚集。为了维持细胞内稳态，氧化蛋白可以通过泛素-蛋白酶体途径或通过自噬在细胞内降解，这取决于细胞的氧化还原状态。或者，细胞可以通过释放细胞外囊泡（EV）来去除氧化蛋白，所述细胞外囊泡（EV）可以转移到邻近或远处的细胞，从而引发细胞间氧化应激反应。在这篇文章中，我们讨论了EV在氧化应激反应中的作用，EV作为氧化应激敏感生物标志物的潜力，以及超氧化物歧化酶在减轻化疗引起的EV相关氧化应激反应中的作用。
The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the drugs approved by the Food and Drug Administration for cancer treatment are associated with the generation of reactive oxygen species, and Doxorubicin (Dox) is one of them. Dox undergoes redox cycling by involving its quinone structure in the production of superoxide free radicals, which are thought to be instrumental to the role it plays in cardiomyopathy. Dox-induced protein oxidation changes protein function, translocation, and aggregation that are toxic to cells. To maintain cellular homeostasis, oxidized proteins can be degraded intracellularly by ubiquitin-proteasome pathway or by autophagy, depending on the redox status of the cell. Alternatively, the cell can remove oxidized proteins by releasing extracellular vesicles (EVs), which can be transferred to neighboring or distant cells, thereby instigating an intercellular oxidative stress response. In this article, we discuss the role of EVs in oxidative stress response, the potential of EVs as sensitive biomarkers of oxidative stress, and the role of superoxide dismutase in attenuating EV-associated oxidative stress response resulting from chemotherapy.
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