Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer.
Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer.
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DOI：
10.1016/j.mrrev.2021.108365
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发表时间：
2021-01
期刊：
影响因子：
--
通讯作者：
Besaratinia A
中科院分区：
文献类型：
--
作者：
Caliri AW;Tommasi S;Besaratinia A
吸烟是多种疾病的主要危险因素，包括癌症和免疫介导的炎症性疾病。烟草烟雾含有多种化学物质的混合物，其中包括大量活性氧和氮物质（ROS和RNS），这些物质可损害细胞和亚细胞靶点，如脂质、蛋白质和核酸。越来越多的证据支持吸烟诱导的ROS和由此产生的氧化应激在炎症和癌变中的关键作用。这篇全面的最新综述涵盖了四个相互关联的主题，包括“吸烟”，“氧化应激”，“炎症”和“癌症”。该综述讨论了四个主题中的每一个，同时通过突出ROS引起的大分子损伤来探索主题之间的交叉点。具体而言，氧化损伤的大分子靶点，如脂质过氧化，蛋白质的翻译后修饰，和DNA加合，以及酶和非酶的抗氧化防御机制，和多方面的修复途径的氧化损伤的描述。还讨论了生物后果的氧化损伤的大分子，如果他们逃避防御机制和/或没有正确或及时修复。重点放在遗传和表观遗传的改变，可能会导致转录失调的功能重要的基因和中断的监管元件。吸烟相关的氧化应激也激活炎症反应途径，这引发了一系列事件，其中ROS的产生是最初但不可或缺的步骤。在损伤和炎症部位释放ROS有助于对抗外来病原体并恢复受损组织，同时增加氧化应激的负担。这产生了一个恶性循环，其中吸烟相关的氧化应激引起炎症，这反过来又导致ROS的进一步产生，并可能增加对大分子靶点的氧化损伤，这可能导致癌症的发生和/或进展。
Smoking is a major risk factor for a variety of diseases, including cancer and immune-mediated inflammatory diseases. Tobacco smoke contains a mixture of chemicals, including a host of reactive oxygen- and nitrogen species (ROS and RNS), among others, that can damage cellular and sub-cellular targets, such as lipids, proteins, and nucleic acids. A growing body of evidence supports a key role for smoking-induced ROS and the resulting oxidative stress in inflammation and carcinogenesis. This comprehensive and up-to-date review covers four interrelated topics, including ‘smoking’, ‘oxidative stress’, ‘inflammation’, and ‘cancer’. The review discusses each of the four topics, while exploring the intersections among the topics by highlighting the macromolecular damage attributable to ROS. Specifically, oxidative damage to macromolecular targets, such as lipid peroxidation, post-translational modification of proteins, and DNA adduction, as well as enzymatic and non-enzymatic antioxidant defense mechanisms, and the multi-faceted repair pathways of oxidized lesions are described. Also discussed are the biological consequences of oxidative damage to macromolecules if they evade the defense mechanisms and/or are not repaired properly or in time. Emphasis is placed on the genetic- and epigenetic alterations that may lead to transcriptional deregulation of functionally-important genes and disruption of regulatory elements. Smoking-associated oxidative stress also activates the inflammatory response pathway, which triggers a cascade of events of which ROS production is an initial yet indispensable step. The release of ROS at the site of damage and inflammation helps combat foreign pathogens and restores the injured tissue, while simultaneously increasing the burden of oxidative stress. This creates a vicious cycle in which smoking-related oxidative stress causes inflammation, which in turn, results in further generation of ROS, and potentially increased oxidative damage to macromolecular targets that may lead to cancer initiation and/or progression.
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