健康成人与伊马替尼治疗的慢性髓性白血病成人患者氧化应激的评估及相关性

Q4 Medicine
B. Labachevski, Marija Popova Labacevska, Irina Panovska Stavridis, S. Trajkova, A. Pivkova Veljanovska, Z. Stojanoski, N. Ridova, D. Zendelovska, M. Petrusevska, T. Balkanov
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引用次数: 0

摘要

活性氧(ROS)是细胞信号传导和其他重要生理功能所必需的含氧自由基。然而,它们的产量增加到过量会导致细胞氧化还原状态的改变,从而连续破坏各种正常的生物功能。氧化应激(OS)发生时,活性氧产生和抗氧化防御机制之间的不平衡。慢性OS导致许多DNA修饰和DNA修复的改变,导致DNA损伤,其中许多可能是有毒和/或致突变的。已证实OS参与慢性髓系白血病(chronic myeloid leukemia, CML)的发病机制。CML是一种骨髓增生性肿瘤,其特征是成熟和成熟髓系细胞不受控制的增殖,其原因是t易位(9;22)导致BCR-ABL融合蛋白异常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ASSESSMENT AND CORELATION OF OXIDATIVE STRESS BETWEEN HEALTHY ADULTS AND ADULT PATIENTS WITH CHRONIC MYELOID LEUKEMIA TREATED WITH IMATINIB
Reactive oxygen species (ROS) are oxygen-containing radicals essential for cell signaling and other vital physiological functions. However, their increased production to an excessive amount can cause alterations in the cellular redox status with consecutive disruption of various normal biological functions. Oxidative stress (OS) occurs when there is an imbalance between ROS production and antioxidant defence mechanisms. Chronic OS results in many DNA modifications, and alterations in DNA repair, leading to DNA lesions of which many can be toxic and/or mutagenic. It is proven that OS is involved in the pathogenesis of chronic myeloid leukaemia (CML), a myeloproliferative neoplasm characterized by uncontrolled proliferation of maturing and mature myeloid cells, caused by the presence of translocation t(9;22) leading to the abnormal BCR-ABL fusion protein.
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