Assessment of genotoxic damage induced by exposure to binary mixtures of polycyclic aromatic hydrocarbons and three heavy metals in male mice.

IF 3.2 4区医学 Q1 Pharmacology, Toxicology and Pharmaceutics

Toxicology Mechanisms and Methods Pub Date : 2024-11-01 Epub Date: 2024-06-11 DOI:10.1080/15376516.2024.2365434

Norberto Alarcón-Herrera, Sandra Gómez-Arroyo, Saúl Flores-Maya, Ana Rosa Flores-Márquez, Paulina Abrica-González

{"title":"Assessment of genotoxic damage induced by exposure to binary mixtures of polycyclic aromatic hydrocarbons and three heavy metals in male mice.","authors":"Norberto Alarcón-Herrera, Sandra Gómez-Arroyo, Saúl Flores-Maya, Ana Rosa Flores-Márquez, Paulina Abrica-González","doi":"10.1080/15376516.2024.2365434","DOIUrl":null,"url":null,"abstract":"Introduction: Heavy metals (HM) and polycyclic aromatic hydrocarbons (PAHs) exposition has been associated with health problems. Therefore, this research evaluated genotoxicity induced in male mice strain CD-1 exposed to benzo[a]anthracene (B[a]A) and benzo[a]pyrene (B[a]P) and their interaction with Fe, Pb, and Al.Methods: Groups of animals were exposed intraperitoneally to HM, PAHs, and mixtures of both. Peripheral blood samples were taken from 0 to 96 h at 24 h intervals; genotoxicity was determined by micronucleus tests and comet assay. Additionally, toxicity and viability were evaluated.Results: HM and PAHs individually were genotoxic. About toxicity, only Al altered polychromatic erythrocytes number and did not change leukocytes viability. Concerning mixtures, Fe + B[a]P, Fe + B[a]A, Pb + B[a]P increased genotoxicity. There were no changes with Pb + B[a]A. Finally, Al mixtures with both PAHs damage was decreased.Conclusions: Exposure to HM and PAH caused genetic damage. Fe, Al, and B[a]A, established a genotoxic potential. Every metal can interact with PAHs in different ways. Also, the micronucleus test and the comet assay demonstrated their high capacity and reliability to determine the genotoxic potential of the compounds evaluated in this work.","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"955-969"},"PeriodicalIF":3.2000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Mechanisms and Methods","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15376516.2024.2365434","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/11 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}

引用次数: 0

Abstract

Introduction: Heavy metals (HM) and polycyclic aromatic hydrocarbons (PAHs) exposition has been associated with health problems. Therefore, this research evaluated genotoxicity induced in male mice strain CD-1 exposed to benzo[a]anthracene (B[a]A) and benzo[a]pyrene (B[a]P) and their interaction with Fe, Pb, and Al.

Methods: Groups of animals were exposed intraperitoneally to HM, PAHs, and mixtures of both. Peripheral blood samples were taken from 0 to 96 h at 24 h intervals; genotoxicity was determined by micronucleus tests and comet assay. Additionally, toxicity and viability were evaluated.

Results: HM and PAHs individually were genotoxic. About toxicity, only Al altered polychromatic erythrocytes number and did not change leukocytes viability. Concerning mixtures, Fe + B[a]P, Fe + B[a]A, Pb + B[a]P increased genotoxicity. There were no changes with Pb + B[a]A. Finally, Al mixtures with both PAHs damage was decreased.

Conclusions: Exposure to HM and PAH caused genetic damage. Fe, Al, and B[a]A, established a genotoxic potential. Every metal can interact with PAHs in different ways. Also, the micronucleus test and the comet assay demonstrated their high capacity and reliability to determine the genotoxic potential of the compounds evaluated in this work.

查看原文本刊更多论文

评估雄性小鼠暴露于多环芳烃和三种重金属的二元混合物诱发的基因毒性损伤。

导言：重金属（HM）和多环芳烃（PAHs）暴露与健康问题有关。因此，本研究评估了暴露于苯并[a]蒽（B[a]A）和苯并[a]芘（B[a]P）的雄性小鼠品系 CD-1 的遗传毒性，以及它们与铁、铅和铝的相互作用：一组动物腹腔暴露于 HM、PAHs 和两者的混合物。每隔 24 小时采集一次 0 至 96 小时的外周血样本；通过微核试验和彗星试验确定遗传毒性。此外，还对毒性和存活率进行了评估：结果：HM 和 PAHs 都具有遗传毒性。在毒性方面，只有 Al 会改变多色红细胞的数量，而不会改变白细胞的活力。关于混合物，Fe + B[a]P、Fe + B[a]A、Pb + B[a]P 会增加基因毒性。而 Pb + B[a]A 则没有变化。最后，含有两种多环芳烃的 Al 混合物对基因的损害有所降低：结论：接触 HM 和 PAH 会造成遗传损伤。铁、铝和 B[a]A 具有潜在的遗传毒性。每种金属都能以不同的方式与多环芳烃相互作用。此外，微核试验和彗星试验也证明了它们在确定本研究中评估的化合物的遗传毒性潜力方面具有很高的能力和可靠性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

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.