E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells

Hyun‐Wook Lee(New York University), Sung‐Hyun Park(New York University), Mao-wen Weng(New York University), Hsiang‐Tsui Wang(New York University), William C. Huang(New York University), Herbert Lepor(New York University), Xue‐Ru Wu(New York University), Lung‐Chi Chen(New York University), Moon-shong Tang(New York University)
Proceedings of the National Academy of Sciences
January 29, 2018
Cited by 357Open Access
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Abstract

Significance E-cigarette smoke (ECS) delivers nicotine through aerosols without burning tobacco. ECS is promoted as noncarcinogenic. We found that ECS induces DNA damage in mouse lung, bladder, and heart and reduces DNA-repair functions and proteins in lung. Nicotine and its nitrosation product 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone can cause the same effects as ECS and enhance mutations and tumorigenic cell transformation in cultured human lung and bladder cells. These results indicate that nicotine nitrosation occurs in the lung, bladder, and heart, and that its products are further metabolized into DNA damaging agents. We propose that ECS, through damaging DNA and inhibiting DNA repair, might contribute to human lung and bladder cancer as well as to heart disease, although further studies are required to substantiate this proposal.


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