Seo Yoon-Seok, Park Jung-Min, Kim Jae-Hyeong, Lee Moo-Yeol
BK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si 10326, Gyeonggi-do, Republic of Korea.
Antioxidants (Basel). 2023 Sep 7;12(9):1732. doi: 10.3390/antiox12091732.
Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species (ROS) is widely accepted as a primary molecular event that predisposes individuals to these smoking-related ailments. This review focused on how cigarette smoke (CS) promotes ROS formation rather than the pathophysiological repercussions of ROS and oxidative stress. A comprehensive analysis of existing studies revealed the following key ways through which CS imposes ROS burden on biological systems: (1) ROS, as well as radicals, are intrinsically present in CS, (2) CS constituents generate ROS through chemical reactions with biomolecules, (3) CS stimulates cellular ROS sources to enhance production, and (4) CS disrupts the antioxidant system, aggravating the ROS generation and its functions. While the evidence supporting these mechanisms is chiefly based on in vitro and animal studies, the direct clinical relevance remains to be fully elucidated. Nevertheless, this understanding is fundamental for deciphering molecular events leading to oxidative stress and for developing intervention strategies to counter CS-induced oxidative stress.
吸烟被认为是多种疾病的重要危险因素，包括心血管疾病、呼吸道疾病和各种癌症。虽然确切的致病机制仍在探索中，但通过产生过量活性氧（ROS）诱导氧化应激被广泛认为是使个体易患这些与吸烟相关疾病的主要分子事件。本综述聚焦于香烟烟雾（CS）如何促进ROS形成，而非ROS和氧化应激的病理生理后果。对现有研究的全面分析揭示了CS给生物系统带来ROS负担的以下关键方式：（1）ROS以及自由基本身存在于CS中，（2）CS成分通过与生物分子的化学反应产生ROS，（3）CS刺激细胞ROS来源以增加产生，以及（4）CS破坏抗氧化系统，加剧ROS生成及其作用。虽然支持这些机制的证据主要基于体外和动物研究，但直接的临床相关性仍有待充分阐明。然而，这种理解对于解读导致氧化应激的分子事件以及制定应对CS诱导氧化应激的干预策略至关重要。
