氧化应激是氧代谢过程中ROS累积，超过抗氧化系统调控能力，诱发细胞功能障碍甚至死亡。
第十七篇：Polyphenols inhibiting MAPK signalling pathway mediated oxidative stress and inflammation in depression[1]
多酚通过抑制MAPK信号通路介导的氧化应激和炎症作用缓解抑郁症。
Schematic illustration of oxidative-induced signaling pathways. Overproduction of ROS results in the activation of NF-кB, MAPK, and PIK/Akt pathways.
Phosphorylation of IкB by IKK results in the release of cytoplasmic NF-кB and subsequently its translocation into the nucleus. In the nucleus, NF-кB activates the expression of the pro-inflammatory gene. NF-кB can also be activated by MAPK and PI3K/Akt pathways.
氧化应激诱导的信号通路示意图。活性氧（ROS）的过度产生会激活NF-κB、MAPK和PI3K/Akt等信号通路。 IKK对IκB的磷酸化导致细胞质中的NF-κB释放，并随后转位进入细胞核。在细胞核内，NF-κB激活促炎基因的表达。
此外，NF-κB也可通过MAPK和PI3K/Akt通路被激活。
Oxidative stress results in the activation of ASK1, an upstream regulator of the MAPK pathway. ROS induces the oxidation of Trx and its dissociation from the ASK1.Trx is ASK1 binding protein and is responsible for its inactivation. TRAF2 and TRAF6 were recruited to ASK1 to form the activated ASK1, after the ROS-induced dissociation of Trx from the ASK1. Furthermore, ASK1 phosphorylates MEKs, which further phosphorylate JNK and p38 MAPK. Activated MAPKs induce the phosphorylation of several transcriptional factors, leading to the regulation of several cellular activities including apoptosis, and inflammation. ROS can also activate MAPK pathways by inhibiting MKPs.
氧化应激会激活MAPK通路的上游调控因子ASK1。ROS可诱导Trx的氧化，并使其从ASK1上解离。Trx是ASK1的结合蛋白，负责抑制其活性。在ROS诱导Trx从ASK1解离后，TRAF2和TRAF6被募集至ASK1，形成活化状态的ASK1复合物。随后，ASK1对MEK蛋白进行磷酸化，进而激活JNK和p38 MAPK。活化的MAPK可磷酸化多个转录因子，从而调控包括细胞凋亡和炎症在内的多种细胞活动。此外，ROS还可通过抑制MAPK磷酸酶（MKPs）进一步激活MAPK信号通路。
Effects of polyphenols on MAPK, NFκB, and PI3K/Akt pathway.
多酚对MAPK、NFκB和PI3K/Akt通路的影响。
第十八篇：Oxidative stress and Parkinson’s disease[2]
氧化应激与帕金森病
Suggested physiological processes related to pathogenesis of Parkinson’s disease (PD).
与帕金森病（PD）发病机制相关的生理过程示意图
第十九篇：Oxidative toxicity in diabetes and Alzheimer’s disease: mechanisms behind ROS/ RNS generation[3]
糖尿病和阿尔茨海默病中的氧化毒性：ROS/RNS 生成背后的机制
ROS production in mitochondria.
线粒体中ROS的产生机制。
Oxidative stress production and damage in T2DM. Hyperglycemia is considered as major contributor in ROS production and associated- damage in T2DM. Induced glucose concentrations may have led to glucose autoxidation, impaired mitochondrial bioenergetics and over production of ROS. Induced oxidative stress in T2DM can impair a couple of transcription factors and pathways like P13K, JAK/STAT, JNK, p-38, ERK/MAPK and CDC42 that resulted in insulin resistance. The other glycolytic intermediates can have led to microvascular complications and endothelial dysfunctions and prone to several diabetic complications.
2型糖尿病（T2DM）中的氧化应激产生与损伤。
高血糖被认为是T2DM中活性氧（ROS）产生及相关损伤的主要诱因。 血糖浓度升高可引发葡萄糖自氧化、线粒体生物能障碍以及ROS的过度产生。 T2DM诱导的氧化应激可损伤多种转录因子及信号通路，如PI3K、JAK/STAT、JNK、p38、ERK/MAPK和CDC42，从而导致胰岛素抵抗。 此外，糖酵解过程中生成的中间代谢产物也可能引发微血管并发症、内皮功能障碍，并促使多种糖尿病相关并发症的发生。
Production and mechanism of oxidative stress in AD. Brain consumes more oxygen than the whole body, and is a rich source of fatty acids and metals that are more susceptible to oxidative damage in AD. Two main hallmarks of AD i.e. Aβ plaques and hyper-phosphorylated tau neurofibrillary tangles (T-NFTs) are involved in production as well as promotion of oxidative damage. Any abnormal increase in ROS due to presence of Aβ and NFTs promote mitochondrial DNA/ RNA damage that resulted in mitochondrial dysfunction and membrane damage. Other damages associated with oxidative stress in AD are autoxidation of glucose that resulted in production of AGES and alternatively induce Aβ- toxicity. As oxidative stress, itself induce Aβ and NFTs formation, the result is induced apoptosis, neuronal death and impaired synapsis.
阿尔茨海默病（AD）中氧化应激的产生与机制。
大脑的耗氧量高于全身其他组织，同时富含易受氧化损伤的脂肪酸和金属元素，因此在AD中更易发生氧化应激。 AD的两个主要特征——Aβ斑块和高磷酸化tau神经原纤维缠结（T-NFTs）不仅参与ROS的生成，也会促进氧化损伤的进展。
Aβ和NFTs的存在可导致ROS异常升高，进而引起线粒体DNA和RNA的损伤，导致线粒体功能障碍和膜损伤。
AD中与氧化应激相关的其他损伤还包括葡萄糖的自氧化，生成晚期糖基化终产物（AGEs），从而进一步诱导Aβ的毒性作用。
由于氧化应激本身也可诱导Aβ和NFTs的形成，最终引发细胞凋亡、神经元死亡和突触功能障碍。
第二十篇：Oxidative Stress in Cardiovascular Diseases[4]
心血管疾病中的氧化应激
ROS formation and detoxification.
ROS的形成和解毒。
Compartmentalization of cardiac antioxidant enzymes.
心脏抗氧化酶的区室化分布。
Physiological roles of oxidative stress in cardiovascular tissues.
氧化应激在心血管组织中的生理作用。
Pathological roles of oxidative stress in cardiovascular tissues.
氧化应激在心血管组织中的病理作用。
参考文献：
[1] T. Behl et al., “Polyphenols inhibiting MAPK signalling pathway mediated oxidative stress and inflammation in depression,” Feb. 01, 2022, Elsevier Masson s.r.l. doi: 10.1016/j.biopha.2021.112545.
[2] J. Blesa, I. Trigo-Damas, A. Quiroga-Varela, and V. R. Jackson-Lewis, “Oxidative stress and Parkinson’s disease,” Jul. 08, 2015, Frontiers Research Foundation. doi: 10.3389/fnana.2015.00091.
[3] W. Ahmad, B. Ijaz, K. Shabbiri, F. Ahmed, and S. Rehman, “Oxidative toxicity in diabetes and Alzheimer ’ s disease : mechanisms behind ROS / RNS generation,” J Biomed Sci, pp. 1–10, 2017, doi: 10.1186/s12929-017-0379-z.
[4] E. Dubois-deruy, V. Peugnet, A. Turkieh, and F. Pinet, “Oxidative Stress in Cardiovascular Diseases,” Antioxidants, 2020.