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Review Article

化疗/放疗致肺毒性中的氧化还原相互作用机制和治疗观点

卷 23, 期 13, 2022

发表于: 26 August, 2022

页: [1261 - 1276] 页: 16

弟呕挨: 10.2174/1389450123666220705123315

价格: $65

摘要

肺毒性是癌症治疗的一个关键限制因素，特别是肺、乳腺和食道恶性肿瘤。胸部和乳房恶性肿瘤的放射治疗可导致肺损伤。然而，全身癌症化疗也可能导致肺肺炎和纤维化。放射治疗直接与细胞内的水分子相互作用产生活性氧(ROS)。然而，放疗和其他治疗方式可能诱导免疫细胞和一些非免疫细胞(如成纤维细胞和内皮细胞)内源性产生ROS和一氧化氮(NO)。肺组织中有几种活性氧生成酶。氧化酶、环氧合酶-2 (COX-2)、双氧化酶(DUOX1和DUOX2)以及线粒体中的细胞呼吸系统是肺暴露于抗癌药物后ROS产生的主要来源。此外，诱导型一氧化氮合酶(iNOS)在放疗或化疗后NO的生成中起关键作用。内皮细胞、成纤维细胞、巨噬细胞和淋巴细胞持续产生ROS和NO，导致细胞凋亡、坏死和衰老，从而释放炎症和促纤维化细胞因子。本文综述了氧化还原引起的肿瘤治疗后肺损伤的细胞和分子机制，并提出了减轻肺毒性的一些靶点和展望。

关键词: 肺，还原/氧化(氧化还原)，肺炎，纤维化，活性氧(ROS)，细胞因子。

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