Evaluation and comparison of DNA alkylation and oxidative damage in e-cigarette and heated tobacco users.

IF 3.2 4区医学 Q1 Pharmacology, Toxicology and Pharmaceutics

Toxicology Mechanisms and Methods Pub Date : 2024-08-13 DOI:10.1080/15376516.2024.2390028

Göksel Koç Morgil, İsmet Çok

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引用次数: 0

Abstract

Objectives: This study, aimed to determine and compare DNA damage in e-cigarette and HTP (IQOS) users by assessing DNA-adducts, which are biomarkers of various DNA alkylation and oxidation.

Methods: For the evaluation of DNA alkylation, N³-Ethyladenine (N³-EtA) and N³-Methyladenine (N³-MeA) adducts were used. DNA oxidation was assessed using, 8-hydroxy-2'-deoxyguanosine(8-OHdG). The urinary cotinine, N³-MeA, N³-EtA, and 8-OHdG concentrations of the cigarette smokers (n:39), e-cigarette users (n:28), IQOS users (n:20), passive smokers (n:32), and nonsmokers(n:41) who lived Ankara, Turkiye were determined using, liquid chromatography-tandem mass spectrometry (LC-MS/MS).

Results: In light of the detected 8-OHdG levels, e-cigarette (3.19 ng/g creatinine) and IQOS (4.38 ng/g creatinine) users had higher oxidative DNA damage than healthy nonsmokers (2.51 ng/g creatinine). Alkylated DNA-adducts were identified in the urine of e-cigarette (N³-MeA: 3.92 ng/g creatinine; N³-EtA: 0.23 ng/g creatinine) and IQOS (N³-MeA: 7.54 ng/g creatinine; N³-EtA: 0.29 ng/g creatinine) users. In the generation of N³-MeA adducts, a significant difference was found between IQOS users and e-cigarette users (p < 0.05). Also, DNA alkylation in flavored e-cigarette users (N³-MeA: 4.51 ng/g creatinine; N³-EtA: 0.27 ng/g creatinine) was higher than in non-flavored e-cigarette users (N³-MeA: 2.27 ng/g creatinine; N³-EtA: 0.06 ng/g creatinine). The highest cotinine levels were found in cigarette smokers (16.1316 ng/g creatinine). No significant difference was found when e-cigarette (1163.02 ng/g creatinine) and IQOS smokers were compared (1088.3 ng/g creatinine).

Conclusion: People who use e-cigarettes and IQOS may be at higher risk of genotoxicity than those who do not use and are not exposed to any tobacco products. Furthermore, the usage of flavoring additives in e-cigarettes contributed to additional genotoxic damage risks.

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评估和比较电子烟和加热烟草使用者的 DNA 烷基化和氧化损伤。

研究目的本研究旨在通过评估作为各种 DNA 烷基化和氧化的生物标志物的 DNA 加合物，确定并比较电子烟和 HTP（IQOS）使用者的 DNA 损伤情况：评估 DNA 烷基化时使用了 N3-乙基腺嘌呤（N3-EtA）和 N3-甲基腺嘌呤（N3-MeA）加合物。DNA 氧化采用 8- 羟基-2'-脱氧鸟苷（8-OHdG）进行评估。使用液相色谱-串联质谱法（LC-MS/MS）测定了居住在土耳其安卡拉的吸烟者（39 人）、电子烟使用者（28 人）、IQOS 使用者（20 人）、被动吸烟者（32 人）和非吸烟者（41 人）的尿液中可替宁、N3-MeA、N3-EtA 和 8-OHdG 的浓度：从检测到的 8-OHdG 水平来看，电子烟（3.19 纳克/克肌酐）和 IQOS（4.38 纳克/克肌酐）使用者的 DNA 氧化损伤高于健康的非吸烟者（2.51 纳克/克肌酐）。在电子烟（N3-MeA：3.92 纳克/克肌酐；N3-EtA：0.23 纳克/克肌酐）和 IQOS（N3-MeA：7.54 纳克/克肌酐；N3-EtA：0.29 纳克/克肌酐）使用者的尿液中发现了烷基化 DNA 加合物。在 N3-MeA 加合物的生成方面，IQOS 用户与电子烟用户之间存在显著差异（P 3-MeA：4.51 纳克/克肌酐；N3-EtA：0.27 纳克/克肌酐），后者高于非香味电子烟用户（N3-MeA：2.27 纳克/克肌酐；N3-EtA：0.06 纳克/克肌酐）。吸烟者的可替宁水平最高（16.1316 纳克/克肌酐）。在比较电子烟（1163.02 纳克/克肌酐）和 IQOS 吸烟者（1088.3 纳克/克肌酐）时，没有发现明显差异：结论：与不使用和不接触任何烟草产品的人相比，使用电子烟和 IQOS 的人可能面临更高的遗传毒性风险。此外，电子烟中香料添加剂的使用也增加了基因毒性损伤的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Toxicology Mechanisms and Methods 医学-毒理学

CiteScore

6.60

自引率

3.10%

发文量

审稿时长

6-12 weeks

期刊介绍： Toxicology Mechanisms and Methods is a peer-reviewed journal whose aim is twofold. Firstly, the journal contains original research on subjects dealing with the mechanisms by which foreign chemicals cause toxic tissue injury. Chemical substances of interest include industrial compounds, environmental pollutants, hazardous wastes, drugs, pesticides, and chemical warfare agents. The scope of the journal spans from molecular and cellular mechanisms of action to the consideration of mechanistic evidence in establishing regulatory policy. Secondly, the journal addresses aspects of the development, validation, and application of new and existing laboratory methods, techniques, and equipment. A variety of research methods are discussed, including: In vivo studies with standard and alternative species In vitro studies and alternative methodologies Molecular, biochemical, and cellular techniques Pharmacokinetics and pharmacodynamics Mathematical modeling and computer programs Forensic analyses Risk assessment Data collection and analysis.