Excessive generation of reactive oxygen species (ROS) in the presence of a defective antioxidant system can induce cellular damage and disrupt normal physiological functions. Several studies have revealed the unfavorable role of ROS in promoting the growth, proliferation, migration, and survival of leukemia cells. In this review study, we summarize the mechanisms of ROS production and its role in leukemogenesis, counteractive effects of antioxidants, and implicate the current ROS-dependent anticancer therapies in acute myeloid leukemia. The dysregulation of the redox system is known to play a significant role in the pathogenesis of leukemia. Leukemia cells generate high levels of ROS, which further increases the levels through extra pathways, including mitochondrial deoxyribonucleic mutation, leukemic oncogene activation, increased nicotinamide adenine phosphate hydrogen (NADPH), and cytochrome P450 activities. Aforementioned pathways once activated have shown to promote genomic instability, induce drug resistance to leukemia medical therapy, disease relapse and reduce survival period. The current standard of treatment with chemotherapy employs the pro-oxidant approach to induce apoptosis and promote tumor regression. However, this approach retains several deleterious effects on the subject resulting in degradation of the quality of life. Nevertheless, the addition of an antioxidant as an adjuvant drug to chemotherapy alleviates treatment-related toxicity, increases chemotherapeutic efficacy, and improves survival rates of a patient. Acute myeloid leukemia remains a daunting challenge to clinicians. The desire to achieve the maximum benefit of chemotherapy but also improve patient outcomes is investigated. ROS generated through several pathways promotes leukemogenesis, drug resistance, and disease relapse. Chemotherapy, the mainstay of treatment, further upregulates ROS levels. Therefore, the addition of an antioxidant to leukemia medical therapy alleviates toxicity and improves patient outcomes.

中文翻译：

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氧化还原系统在髓样白血病中的重要作用：从发病机理到治疗应用

在抗氧化剂系统存在缺陷的情况下，过量产生活性氧（ROS）会诱导细胞损伤并破坏正常的生理功能。多项研究表明，ROS在促进白血病细胞的生长，增殖，迁移和存活中起不利的作用。在这篇综述研究中，我们总结了ROS产生的机制及其在白血病发生中的作用，抗氧化剂的反作用作用，并暗示了目前急性髓细胞白血病中ROS依赖的抗癌治疗方法。已知氧化还原系统的失调在白血病的发病机理中起重要作用。白血病细胞产生高水平的活性氧，从而通过额外的途径进一步提高血红素水平，包括线粒体脱氧核糖核酸突变，白血病致癌基因激活，增加烟酰胺磷酸腺嘌呤氢（NADPH）和细胞色素P450活性。一旦激活，上述途径已显示出可促进基因组不稳定，诱导对白血病药物治疗的耐药性，疾病复发并缩短生存期。当前化学疗法的治疗标准采用促氧化剂方法来诱导细胞凋亡并促进肿瘤消退。但是，这种方法对受试者保留了几种有害作用，导致生活质量下降。然而，在化学疗法中添加抗氧化剂作为辅助药物可减轻与治疗有关的毒性，增加化学疗法的效力，并提高患者的存活率。急性髓细胞白血病仍然是临床医生面临的艰巨挑战。研究了实现最大的化疗获益并改善患者预后的愿望。通过多种途径产生的ROS促进白血病的生成，耐药性和疾病复发。化学疗法是治疗的主要手段，它进一步上调了ROS水平。因此，在白血病药物治疗中添加抗氧化剂可减轻毒性并改善患者预后。