Toxicology Mechanisms and Methods最新文献

{"title":"Mechanistic paradigms of immunotoxicity, triggered by nanoparticles - a review.","authors":"S V S Rana","doi":"10.1080/15376516.2024.2431687","DOIUrl":"10.1080/15376516.2024.2431687","url":null,"abstract":"<p><p>Nanoparticles (NPs) possess the ability to penetrate cells and elicit a rapid and targeted immune response, influenced by their distinct physicochemical properties. These particles can engage with both micro and macromolecules, thereby impacting various downstream signaling pathways that may lead to cell death. This review provides a comprehensive overview of the primary mechanisms contributing to the immunotoxicity of both organic and inorganic nanoparticles. The effects of carbon-based nanomaterials (CNMs), including single-walled carbon nanotubes, multi-walled carbon nanotubes, graphene, and metal oxide nanoparticles, on various immune cell types such as macrophages, neutrophils, monocytes, dendritic cells (DCs), antigen-presenting cells (APCs), and RAW 264.7 cells are examined. The immune responses discussed encompass inflammation, oxidative stress, autophagy, and apoptosis. Additionally, the roles of pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and IFN-γ, along with JAK/STAT signaling pathways, are highlighted. The interaction of NPs with oxidative stress pathways, including MAPK signaling and Nrf2/ARE signaling, is also explored. Furthermore, the mechanisms by which nanoparticles induce damage to organelles such as lysosomes, the endoplasmic reticulum, exosomes, and Golgi bodies within the immune system are addressed. The review also emphasizes the genotoxic and epigenetic mechanisms associated with the immunotoxicity of NPs. Recent advancements regarding the immunotherapeutic potential of engineered NPs are reported. The roles of autophagy and apoptosis in the immunotoxicity of NPs merit further investigation. In conclusion, understanding how engineered nanoparticles modulate immune responses may facilitate the prevention and treatment of human diseases, including cancer and autoimmune disorders.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"262-278"},"PeriodicalIF":3.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disposable electronic cigarettes - chemical composition and health effects of their use. A systematic review.","authors":"Paulina Natalia Kopa-Stojak, Rafal Pawliczak","doi":"10.1080/15376516.2024.2423927","DOIUrl":"10.1080/15376516.2024.2423927","url":null,"abstract":"<p><strong>Objective: </strong>Despite the rising popularity of disposable e-cigarettes, little is known about their chemical characteristics, or their impact on users' health. This work attempts to summarize current knowledge about chemical composition and known health effects of disposable e-cigarettes.</p><p><strong>Methods: </strong>The literature search was performed in February and March 2024 in Pub Med and Science Direct databases (no time range) by the terms 'disposable electronic cigarette', 'disposable e-cigarette', 'disposable e-cigs', 'cig-a-like e-cigarette', 'cig-a-like electronic cigarette'.</p><p><strong>Results: </strong>Disposable e-cigarettes contain: nicotine, humectants (propylene glycol, glycerin), flavoring agents (diacetyl, acetoin, triacetin, p-menthone, triethyl citrate, ethyl maltol, 3-hexen-1-ol, methyl anthranilate, α-terpineol, perillartine, benzyl alcohol, vanillin, melonal, methyl dihydrojasmonate, and γ-decalactone), cooling agents (WS-3, WS-23, menthol), carbonyl compounds (acetaldehyde, formaldehyde, propionaldehyde, acetone, acrolein) volatile organic compounds (VOCs) (benzene, ethanol, methanol, styrene, acetylpirazine and 2,3,5-trimethylpyrazine), metals and inorganic compounds (chromium, nickel, manganese, lead, aluminum, and zinc) and reactive oxygen species. Furthermore, there was some evidence of nicotine dependence, risk of cancer and adverse respiratory effects of using disposable e-cigarettes.</p><p><strong>Conclusions: </strong>Despite the fact that disposable e-cigarettes contain significantly less toxins compared to combustible cigarettes, they include compounds that are absent in such products that may provide health risk in prolonged usage. In addition, there is a limited number of data on the health effect of disposable e-cigarettes, especially in long time period, for never-smokers. Therefore, due to growing popularity of disposable e-cigarettes among young people, who choose them when initiating nicotine use, further research on their long-term impact of on the users' health is necessary.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"250-261"},"PeriodicalIF":3.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative methods for the risk assessment of drinking water contact chemicals following the NSF/ANSI/CAN 600 standard - part I: general methods.","authors":"Bradley J Lampe, Shannon Cousineau, J Caroline English, Shannon Ethridge, Lynne T Haber, Kristin Kerstens, Craig Rowlands, Kelly A Magurany","doi":"10.1080/15376516.2025.2463487","DOIUrl":"https://doi.org/10.1080/15376516.2025.2463487","url":null,"abstract":"<p><p>Health-based criteria have been developed using quantitative methods for over 370 unregulated chemicals that have been detected in extraction testing of products certified or undergoing certification to public health-based drinking water standards. These criteria are derived in accordance with the requirements of NSF/ANSI/CAN 600, <i>Health Effects Evaluation and Criteria for Chemicals in Drinking Water</i> and undergo external peer review by an independent Health Advisory Board. However, a complete and unified description of how these criteria are derived is not available in the scientific literature. This is the first part of a two-part publication that describes the core concepts involved in deriving these criteria. In this first part, general approaches that are consistently applied to the derivation of health-based criteria are discussed, including methods related to the literature search, evaluation of study quality, derivation of the reference dose, selection of uncertainty factors, and identification of the appropriate drinking water intake rate.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-16"},"PeriodicalIF":3.2,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular heterogeneity in pediatric sepsis: identification of oxidative stress-related subtypes and diagnostic biomarkers through integrated bioinformatics analysis.","authors":"Ding Ding, Min Zhang, Zhen Li, Zhengxiang Liu, Nian Liu","doi":"10.1080/15376516.2025.2466577","DOIUrl":"10.1080/15376516.2025.2466577","url":null,"abstract":"<p><strong>Background: </strong>Pediatric sepsis is a life-threatening condition characterized by a dysregulated immune response to infection, often involving heightened oxidative stress. Understanding the molecular heterogeneity of sepsis can provide insights into potential therapeutic targets and diagnostic biomarkers.</p><p><strong>Methods: </strong>Machine learning approaches were employed to identify diagnostic biomarkers. Unsupervised clustering was performed to identify distinct sepsis subtypes. We conducted an integrative analysis combining Gene Set Variation Analysis (GSVA), Gene Set Enrichment Analysis (GSEA), differential gene expression, and functional enrichment to study oxidative stress-related subgroups in sepsis patients. Immune cell infiltration and immune-related pathway activities were analyzed using the ssGSEA algorithm. GSVA and GSEA indicated significant enrichment of oxidative stress-related pathways in sepsis patients compared to controls.</p><p><strong>Results: </strong>Differential expression analysis identified 371 upregulated and 304 downregulated genes in sepsis, with 34 genes linked to oxidative stress. LASSO and Random Forest analyses highlighted key diagnostic genes (GBA and MGST1), validated in independent datasets (GSE13904) with high diagnostic accuracy (AUC: GBA = 0.924, MGST1 = 0.857). Unsupervised clustering revealed two distinct sepsis subtypes with differential immune cell infiltration and pathway activities: Subtype 1 showed higher T cell and TFH infiltration, while Subtype 2 exhibited increased macrophage infiltration. Functional enrichment and GSEA identified key metabolic, oxidative stress, and immune pathways that were enriched in Subtype 2.</p><p><strong>Conclusion: </strong>Our comprehensive bioinformatics analysis unveils significant oxidative stress-related molecular heterogeneity in sepsis, identifying potential diagnostic biomarkers and therapeutic targets. Personalized medicine approaches targeting specific oxidative stress pathways and immune responses could enhance sepsis management and patient outcomes.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-13"},"PeriodicalIF":3.2,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network toxicology analysis reveals molecular mechanisms associated with noise exposure to multiple diseases.","authors":"Maria Taboada-Alquerque, Jesus Olivero-Verbel","doi":"10.1080/15376516.2025.2460591","DOIUrl":"10.1080/15376516.2025.2460591","url":null,"abstract":"<p><p>Noise pollution is recognized as an environmental stressor that affects various biological processes beyond auditory functions, mainly through stress hormones release. This work explored the biological processes, diseases attributable to noise-regulated targets, and the main targets involved in each disease, employing a network toxicology approach. Through various databases and bioinformatics analysis, a total of 577 targets were identified as potential candidates implicated in diseases related to noise exposure, 10 from the GEO database and the rest from other databases. Noise pollution was found to regulate processes such as hormone response, cellular response to cytokines, and circulatory system functions, contributing to the development of the pathological manifestations related to the diseases like hypertension, ischemia, atherosclerosis, and cirrhosis. Hub targets for ischemia included IL-6, CASP3, AKT1, and TNF-α, while NOS3 was related to hypertension, and NOS3, TNF-α, AGT, and IL-1B to atherosclerosis. The targets were found to be linked to vascular regulation and inflammation in cardiovascular and cerebrovascular diseases. Molecular docking studies indicated stress hormones released by noise exposure regulates these diseases through signaling pathways, without implicating its direct binding to hub targets. The results indicate that individuals with vascular diseases are more vulnerable to the effects of prolonged noise exposure.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-16"},"PeriodicalIF":3.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in heavy metal detection using microneedle array technology.","authors":"Robert M Taylor, Abdul-Mehdi S Ali, Yiliang Zhu, Alicia M Bolt, Justin T Baca","doi":"10.1080/15376516.2025.2461647","DOIUrl":"10.1080/15376516.2025.2461647","url":null,"abstract":"<p><p>Heavy metal and metalloid (HM) exposure poses significant health risks, including cardiovascular disease, cancer, and renal damage. This contamination, prevalent in the Western US, involves arsenic (As), cadmium (Cd), uranium (U), and vanadium (V). Interstitial fluid (ISF) is a source of biomarkers, which can be minimally invasively collected using microneedle array (MA) technology. Our study hypothesized that MA-extracted ISF would facilitate noninvasive HM quantification. We established analytical parameters for HM detection in ISF using inductively coupled plasma-mass spectrometry (ICP-MS), defined baseline ISF HM concentrations in unexposed animal populations, and monitored HM levels in ISF under mixed exposure in animal models. Additionally, we assessed HM levels in ISF and biological fluids from three human subjects. Thirty-six Sprague-Dawley rats were divided into cohorts: low-level mixed HMs exposure (5X maximum contaminant level (MCL)); high-level single HM with low-level others (50X MCL for one HM with 5X for others); and unexposed controls. ISF and plasma were collected weekly for 8 weeks and analyzed <i>via</i> ICP-MS. Our findings reveal a correlation between ISF and plasma HM levels, underscoring ISF's potential for real-time monitoring of HM exposure. This study also establishes baseline ISF HM levels, illustrating the feasibility of HM quantification using small ISF volumes.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brij 35 inhibited the CYP2E1-mediated metabolism and P-gp mediated transport of paracetamol in rats and <i>in vitro</i> models: amelioration of paracetamol toxicity.","authors":"Nagabhushanam Chunduru, Ravindra Babu Pingili, Vijaya R Dirisala, Prasad K","doi":"10.1080/15376516.2025.2457331","DOIUrl":"10.1080/15376516.2025.2457331","url":null,"abstract":"<p><p>The harmful by-product of paracetamol is known as N-Acetyl-p-benzoquinoneimine, (NAPQI). When paracetamol is given at therapeutic dosages or in excess, it undergoes Phase I metabolism in the liver <i>via</i> Cytochrome P-450 2E1 (CYP2E1), and then it produces NAPQI. Previous studies reported that a nonionic surfactant known as Brij 35 (Polyoxyethylene lauryl ether) has been shown to be an effective inhibitor of CYP2E1 and P-glycoprotein (P-gp). Hence, this <i>in vitro</i> and <i>in vivo</i> investigation set out to assess Brij 35 impact on paracetamol CYP2E1-mediated metabolism. For the <i>in vitro</i> investigation, isolated rat hepatocytes were used. Male Wistar rats were used for <i>in vivo</i> studies. There were 30 rats in total, with six individuals each group distributed among the five groups. The first group animals received 0.5% sodium carboxy methyl cellulose (control group); the second group animals treated with 300 mg/kg of paracetamol; the third group animals treated with Brij 35 (5 mg/kg) along with 300 mg/kg of paracetamol; the fourth group animals treated with 10 mg/kg of Brij 35 along with 300 mg/kg of paracetamol, and the fifth group animals treated with 20 mg/kg of Brij 35 along with 300 mg/kg of paracetamol for consecutive 21 days. The current study found that paracetamol plasma concentrations were much higher and NAPQI plasma concentrations were much lower when Brij 35 was co-administered may be due to inhibition of CYP2E1-mediated metabolism and P-gp-mediated intestinal transport of paracetamol. Brij 35 also reduced the increased hepatic and renal markers with significant hepatoprotective and nephroprotective changes in the histopathological investigation.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-10"},"PeriodicalIF":3.2,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms involved in the valproic acid-induced hepatotoxicity: a comprehensive review.","authors":"Rohan Kadam, Mahesh Palkar, Ravindra Babu Pingili","doi":"10.1080/15376516.2025.2459176","DOIUrl":"10.1080/15376516.2025.2459176","url":null,"abstract":"<p><p>Adverse drug reactions (ADR) remain a challenge in modern healthcare, particularly given the increasing complexity of therapeutics. An anticonvulsant medicine which is frequently used in treatment of epilepsy and other neurological conditions is valproic acid (VPA), is frequently associated with hepatotoxicity, a severe ADR that complicates its clinical use, which can take two different forms: Type I, which is defined by dose-dependent and reversible liver damage, and Type II, an idiosyncratic reaction that can result in severe liver failure, frequently complicates its clinical application. Oxidative stress, the creation of reactive metabolites, mitochondrial dysfunction, carnitine shortage, immune-mediated reactions, glutathione depletion, and blockage of the bile salt export pump (BSEP) are some of the numerous underlying mechanisms of VA-induced hepatic damage. The production of reactive oxygen species and the liver's antioxidant protection are out of balance as a cause of oxidative stress, which is a significant factor in VPA intoxication. VPA can also accelerate the build-up of fatty acids, which increases the risk of steatosis, due to its interaction with the metabolism of carnitine. Immune-mediated processes have been shown to increase liver injury, implying that the immunity system may possibly be involved in VPA hepatotoxicity. Hepatocyte injury and cholestasis are caused by BSEP inhibition, which impairs bile flow. The complex interaction between biochemical and cellular mechanisms that underlie valproic acid's hepatotoxic potential calls for additional research to clarify the precise pathways implicated and create mitigation techniques for this ADR.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-16"},"PeriodicalIF":3.2,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and safety outcomes associated with aristolochic acid exposure: a systematic review and meta-analysis.","authors":"Ting Cui, Shumei Che, Xingxu Yan, Rongrong Yang, Zhenna Xu, Sijia Liu, Ying Li, Chenyu Hao, Junhan Jiang, Lili Song, Hua Jin, Yubo Li","doi":"10.1080/15376516.2025.2457340","DOIUrl":"10.1080/15376516.2025.2457340","url":null,"abstract":"<p><p>Current studies have clearly shown that aristolochic acid (AA) exposure can induce a variety of diseases, such as kidney disease, liver cancer, and urinary tract cancer (UTC). However, no studies have systematically analyzed and integrated these results. Therefore, we aimed to elucidate the association between AA exposure and the risk of safety outcomes for AA-related overall disease and different types of disease it causes. We conducted an exhaustive search of PubMed, EMBASE, Web of Science, and the Cochrane Library for relevant material up to April 2024. For AA-related overall disease, AA exposure was significantly associated with an increased incidence of AA-related overall disease (OR: 1.289, 95% CI: 1.183-1.404). For different types of disease, AA exposure was significantly associated with increased incidence of kidney disease (OR: 1.279, 95% CI: 1.029-1.590), UTC (OR: 1.842, 95% CI: 1.376-2.465), and liver cancer (OR: 1.146, 95% CI: 1.040-1.262). No significant association was found between AA exposure and the incidence of brain disease (OR: 1.161, 95% CI: 0.989-1.362). This study systematically analyzed various safety outcomes associated with AA exposure to provide a solid scientific basis for future prevention strategies and clinical management.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-11"},"PeriodicalIF":3.2,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation and comparison of DNA alkylation and oxidative damage in e-cigarette and heated tobacco users.","authors":"Göksel Koç Morgil, İsmet Çok","doi":"10.1080/15376516.2024.2390028","DOIUrl":"10.1080/15376516.2024.2390028","url":null,"abstract":"<p><strong>Objectives: </strong>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.</p><p><strong>Methods: </strong>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).</p><p><strong>Results: </strong>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 (<i>p</i> < 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).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"125-135"},"PeriodicalIF":3.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141976701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}