Cancer and Alzheimer’s disease (AD) are characterized by (i) opposing biological mechanisms, (ii) an inverse correlation between their incidences, and (iii) oxidative stress being a common denominator of both diseases. Increased formation of reactive oxygen species (ROS) in cancer cells from oncogenic signaling and/or metabolic disturbances leads to upregulation of cellular antioxidant capacity to maintain ROS levels below a toxic threshold. Combining drugs that induce high levels of ROS with compounds that suppress cellular antioxidant capacity by depleting antioxidant systems [glutathione (GSH), superoxide dismutase (SOD), and thioredoxin (TRX)] and/or targeting glucose metabolism represents a potential anticancer strategy. In AD, free metals and/or Aβ:metal complexes may cause damage to biomolecules in the brain (via Fenton reaction), including DNA. Metal chelation, based on the application of selective metal chelators or metal delivery, may induce neuroprotective signaling and represents a promising therapeutic strategy. This review examines therapeutic strategies based on the modulation of oxidative stress in cancer and AD.

癌症和阿尔茨海默氏病（AD）的特征是（i）相互对立的生物学机制，（ii）发病率之间呈负相关，并且（iii）氧化应激是这两种疾病的共同特征。由于致癌信号和/或代谢紊乱，癌细胞中活性氧种类（ROS）形成的增加导致细胞抗氧化剂的能力上调，以将ROS维持在毒性阈值以下。通过降低抗氧化剂系统[谷胱甘肽（GSH），超氧化物歧化酶（SOD）和硫氧还蛋白（TRX）]和/或靶向葡萄糖代谢，将诱导高水平ROS的药物与抑制细胞抗氧化能力的化合物结合起来，是一种潜在的抗癌策略。在AD中，游离金属和/或Aβ：金属络合物可能会对大脑中的生物分子造成损害（通过Fenton反应），包括DNA。基于选择性金属螯合剂或金属递送的应用，金属螯合可诱导神经保护性信号传导，代表了一种有前途的治疗策略。这项审查审查了基于癌症和AD氧化应激调节的治疗策略。