烟草吸食的魅力在于吸入尼古丁后能够立刻满足人的享乐欲。然而，烟草在烘烤和燃烧过程中会产生很多突变原，其中包括70多种致癌物质。烟草烟雾中存在两种类型的突变原和致癌物质：直接损伤DNA的致癌物和需要代谢激活才能损伤DNA的前致癌物。最近的研究提供了对于烟草烟雾引发DNA损伤的三个新见解。首先，烟草烟雾中的直接致癌物醛类化合物，而不是前致癌物多环芳烃和芳香胺，引起了两种主要类型的DNA损伤：环状-1，N2-羟基-去氧鸟苷（γ-OH-PdG）和α-甲基-1，N2-γ-OH-PdG。其次，烟草烟雾降低了DNA修复蛋白和活性水平，同时醛类化合物也阻止前致癌物的激活。基于这些发现，我们提出醛类化合物是烟草烟雾引起DNA损伤以及致癌的主要来源之一。电子烟（E-cig）旨在以气溶胶形式释放尼古丁而不燃烧烟草。电子烟气溶胶（ECA）含有尼古丁、丙二醇和植物甘油。在小鼠的肺、心脏和膀胱组织中，ECA能够引起O6-甲基脱氧胞嘧啶（O6-medG）和环状γ-羟基-1，N2-丙烷基dG（γ-OH-PdG）的产生，并导致肺部DNA修复蛋白和活性水平降低。尼古丁和尼古丁衍生的亚硝基烯酮（NNK）在人类细胞中产生相同类型的DNA加合物并抑制DNA修复。长期接触后，ECA在小鼠体内可引起肺腺癌和膀胱尿道上皮增生。因此，本文综述了最新关于小鼠和培养人类细胞中尼古丁和ECA所产生的DNA加合物和DNA修复抑制的文献，并提供了有关ECA的致癌性的一些见解。版权所有©2021 Elsevier B.V.

The allure of tobacco smoking is linked to the instant gratification provided by inhaled nicotine. Unfortunately, tobacco curing and burning generates many mutagens including more than 70 carcinogens. There are two types of mutagens and carcinogens in tobacco smoke (TS): direct DNA damaging carcinogens and procarcinogens, which require metabolic activation to become DNA damaging. Recent studies provide three new insights on TS-induced DNA damage. First, two major types of TS DNA damage are induced by direct carcinogen aldehydes, cyclic-1,N2-hydroxy-deoxyguanosine (γ-OH-PdG) and α-methyl-1, N2-γ-OH-PdG, rather than by the procarcinogens, polycyclic aromatic hydrocarbons and aromatic amines. Second, TS reduces DNA repair proteins and activity levels. TS aldehydes also prevent procarcinogen activation. Based on these findings, we propose that aldehydes are major sources of TS induce DNA damage and a driving force for carcinogenesis. E-cigarettes (E-cigs) are designed to deliver nicotine in an aerosol state, without burning tobacco. E-cigarette aerosols (ECAs) contain nicotine, propylene glycol and vegetable glycerin. ECAs induce O6-methyl-deoxyguanosines (O6-medG) and cyclic γ-hydroxy-1,N2--propano-dG (γ-OH-PdG) in mouse lung, heart and bladder tissues and causes a reduction of DNA repair proteins and activity in lungs. Nicotine and nicotine-derived nitrosamine ketone (NNK) induce the same types of DNA adducts and cause DNA repair inhibition in human cells. After long-term exposure, ECAs induce lung adenocarcinoma and bladder urothelial hyperplasia in mice. We propose that E-cig nicotine can be nitrosated in mouse and human cells becoming nitrosamines, thereby causing two carcinogenic effects, induction of DNA damage and inhibition of DNA repair, and that ECA is carcinogenic in mice. Thus, this article reviews the newest literature on DNA adducts and DNA repair inhibition induced by nicotine and ECAs in mice and cultured human cells, and provides insights into ECA carcinogenicity in mice.Copyright © 2021 Elsevier B.V. All rights reserved.