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DNA damage, DNA repair and carcinogenicity: Tobacco smoke versus electronic cigarette aerosol
Moon-Shong Tang1, Hyun-Wook Lee1, Mao-Wen Weng1
1Department of Environmental Medicine, Pathology and Medicine, United States.
Abstract:
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.
Insights
Tobacco smoke aldehydes cause DNA damage and inhibit repair, driving cancer. E-cigarette aerosols also induce DNA damage and inhibit repair, suggesting they are carcinogenic.
Area of Science:
- Toxicology
- Molecular Biology
- Carcinogenesis
Background:
- Tobacco smoking delivers nicotine but generates mutagens and carcinogens.
- Tobacco smoke contains direct-acting carcinogens and procarcinogens requiring metabolic activation.
- Recent research offers new insights into tobacco smoke-induced DNA damage mechanisms.
Purpose of the Study:
- To review new literature on DNA adducts and DNA repair inhibition induced by nicotine and e-cigarette aerosols (ECAs).
- To provide insights into the carcinogenicity of ECAs in mice.
- To elucidate the role of aldehydes in tobacco smoke-induced DNA damage and carcinogenesis.
Main Methods:
- Analysis of DNA damage, specifically DNA adducts like cyclic-1,N2-hydroxy-deoxyguanosine (γ-OH-PdG) and α-methyl-1, N2-γ-OH-PdG, in relation to tobacco smoke exposure.
- Assessment of DNA repair protein and activity levels following exposure to tobacco smoke and ECAs.
- Investigation of DNA adduct formation (O6-methyl-deoxyguanosines and γ-OH-PdG) and DNA repair inhibition in mouse tissues and human cells exposed to ECAs, nicotine, and NNK.
- Evaluation of long-term effects of ECA exposure, including tumor formation and hyperplasia in mice.
Main Results:
- Tobacco smoke aldehydes, not procarcinogens, are major inducers of specific DNA damage (γ-OH-PdG).
- Tobacco smoke reduces DNA repair capacity and aldehydes can inhibit procarcinogen activation.
- ECAs induce specific DNA adducts (O6-medG, γ-OH-PdG) in mouse tissues and reduce DNA repair in lungs.
- Nicotine and NNK induce similar DNA adducts and inhibit DNA repair in human cells.
- Long-term ECA exposure leads to lung adenocarcinoma and bladder hyperplasia in mice.
- ECA is proposed to be carcinogenic in mice due to nicotine nitrosation into carcinogens.
Conclusions:
- Aldehydes in tobacco smoke are identified as primary drivers of DNA damage and carcinogenesis.
- E-cigarette aerosols, containing nicotine, also induce DNA damage and inhibit DNA repair mechanisms.
- Nicotine in ECAs can be nitrosated, leading to carcinogenic effects including DNA damage and repair inhibition.
- The findings suggest that e-cigarette aerosols possess carcinogenic potential in mice.
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