Environmental and Molecular Mutagenesis最新文献

{"title":"Functional roles and cancer variants of the bifunctional glycosylase NEIL2","authors":"Anh B. Hua,&nbsp;Joann B. Sweasy","doi":"10.1002/em.22555","DOIUrl":"10.1002/em.22555","url":null,"abstract":"<p>Over 70,000 DNA lesions occur in the cell every day, and the inability to properly repair them can lead to mutations and destabilize the genome, resulting in carcinogenesis. The base excision repair (BER) pathway is critical for maintaining genomic integrity by repairing small base lesions, abasic sites and single-stranded breaks. Monofunctional and bifunctional glycosylases initiate the first step of BER by recognizing and excising specific base lesions, followed by DNA end processing, gap filling, and finally nick sealing. The Nei-like 2 (NEIL2) enzyme is a critical bifunctional DNA glycosylase in BER that preferentially excises cytosine oxidation products and abasic sites from single-stranded, double-stranded, and bubble-structured DNA. NEIL2 has been implicated to have important roles in several cellular functions, including genome maintenance, participation in active demethylation, and modulation of the immune response. Several germline and somatic variants of NEIL2 with altered expression and enzymatic activity have been reported in the literature linking them to cancers. In this review, we provide an overview of NEIL2 cellular functions and summarize current findings on NEIL2 variants and their relationship to cancer.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"65 S1","pages":"40-56"},"PeriodicalIF":2.8,"publicationDate":"2023-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/em.22555","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9676036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The aflatoxin B1-induced imidazole ring-opened guanine adduct: High mutagenic potential that is minimally affected by sequence context","authors":"Irina G. Minko,&nbsp;Andrew H. Kellum Jr.,&nbsp;Michael P. Stone,&nbsp;R. Stephen Lloyd","doi":"10.1002/em.22556","DOIUrl":"10.1002/em.22556","url":null,"abstract":"<p>Dietary exposure to aflatoxin B₁ (AFB₁) is a recognized risk factor for developing hepatocellular carcinoma. The mutational signature of AFB₁ is characterized by high-frequency base substitutions, predominantly G&gt;T transversions, in a limited subset of trinucleotide sequences. The 8,9-dihydro-8-(2,6-diamino-4-oxo-3,4-dihydropyrimid-5-yl-formamido)-9-hydroxyaflatoxin B₁ (AFB₁-FapyGua) has been implicated as the primary DNA lesion responsible for AFB₁-induced mutations. This study evaluated the mutagenic potential of AFB₁-FapyGua in four sequence contexts, including hot- and cold-spot sequences as apparent in the mutational signature. Vectors containing site-specific AFB₁-FapyGua lesions were replicated in primate cells and the products of replication were isolated and sequenced. Consistent with the role of AFB₁-FapyGua in AFB₁-induced mutagenesis, AFB₁-FapyGua was highly mutagenic in all four sequence contexts, causing G&gt;T transversions and other base substitutions at frequencies of ~80%–90%. These data suggest that the unique mutational signature of AFB₁ is not explained by sequence-dependent fidelity of replication past AFB₁-FapyGua lesions.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"65 S1","pages":"9-13"},"PeriodicalIF":2.8,"publicationDate":"2023-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10711146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9683732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A scoping review of recent advances in the application of comet assay to Allium cepa roots","authors":"Carlotta Alias,&nbsp;Ilaria Zerbini,&nbsp;Donatella Feretti","doi":"10.1002/em.22553","DOIUrl":"10.1002/em.22553","url":null,"abstract":"<p>The comet assay is a sensitive method for the evaluation of DNA damages and DNA repair capacity at single-cell level. <i>Allium cepa</i> is a well-established plant model for toxicological studies. The aim of this scoping review was to investigate the recent application of the comet assay in <i>Allium cepa</i> root cells to assess the genotoxicity. To explore the literature a search was performed selecting articles published between January 2015 and February 2023 from Web of Science, PubMed, and Scopus databases using the combined search terms “Comet assay” and “<i>Allium cepa</i>”. All the original articles that applied the comet assay to <i>Allium cepa</i> root cells were included. Of the 334 records initially found, 79 articles were identified as meeting the inclusion criteria. Some studies reported results for two or more toxicants. In these cases, the data for each toxicant were treated separately. Thus, the number of analyzed toxicants (such as chemicals, new materials, and environmental matrices) was higher than the number of selected papers and reached 90. The current use of the <i>Allium</i>-comet assay seems to be directed towards two types of approach: the direct study of the genotoxicity of compounds, mainly biocides (20% of analyzed compounds) and nano- and microparticles (17%), and assessing a treatment's ability to reduce or eliminate genotoxicity of known genotoxicants (19%). Although the genotoxicity identified by the <i>Allium</i>-comet assay is only one piece of a larger puzzle, this method could be considered a useful tool for screening the genotoxic potential of compounds released into the environment.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"264-281"},"PeriodicalIF":2.8,"publicationDate":"2023-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/em.22553","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9678868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ASIP gene polymorphism associated with black coat and skin color in Murrah buffalo","authors":"Namita Kumari,&nbsp;Rashi Vasisth,&nbsp;Ankita Gurao,&nbsp;Manishi Mukesh,&nbsp;Vikas Vohra,&nbsp;Sanjay Kumar,&nbsp;Ranjit Singh Kataria","doi":"10.1002/em.22554","DOIUrl":"10.1002/em.22554","url":null,"abstract":"<p>The melanogenesis pathway regulates pigmentation through the synergic action of various genes. We are interested in analyzing the genetic variations in the ASIP which determine eumelanin production in the dermis layer. In the present study, the <i>ASIP</i> gene was characterized in buffalo and 268 genetically unrelated buffaloes belonging to 10 different populations were genotyped for the non-synonymous SNP (c.292C&gt;T) identified in the exon 3 region of the gene using Tetra-ARMS-PCR. The TT genotype occurred at a higher rate in Murrah, followed by Nili Ravi, Tripura, and Paralakhemundi (42.63%, 19.30%, 3.45%, and 3.33%). These results convey the association of the black coat color of Murrah with the <i>ASIP</i> gene TT genotype and the lighter shades of black coat (brown and grayish-black) color phenotype in other breeds with the CC genotype.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"309-314"},"PeriodicalIF":2.8,"publicationDate":"2023-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732486","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":"Erratum to “Genotoxic repercussion of high-intensity radiation (x-rays) on hospital radiographers”","authors":"","doi":"10.1002/em.22542","DOIUrl":"10.1002/em.22542","url":null,"abstract":"<p>Kuchi Bhotla, H., Balasubramanian, B., Rengasamy, K.R.R., Arumugam, V.A., Alagamuthu, K.K., Chithravel, V. et al. (2023) Genotoxic repercussion of high-intensity radiation (x-rays) on hospital radiographers. <i>Environmental and Molecular Mutagenesis</i>, 64(2), 123–131.</p><p>In the original article the Ethics approval section has not been included. The Ethics approval section should read as follows:</p><p><b>ETHICS APPROVAL STATEMENT</b></p><p>The study was approved and got its ethical clearance from the Institutional committee from Christ University (Ethical Reference No. ECR/793/Inst/KA/2015/RR-18) and followed the protocols of ethical standards of Declaration of Helsinki 1964, WMA, 2000.</p><p>We apologize for this error.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"321"},"PeriodicalIF":2.8,"publicationDate":"2023-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/em.22542","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9658858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A study on Amygdalin's genotoxicological safety and modulatory activity in human peripheral lymphocytes in vitro","authors":"Esra Erikel,&nbsp;Deniz Yuzbasioglu,&nbsp;Fatma Unal","doi":"10.1002/em.22543","DOIUrl":"10.1002/em.22543","url":null,"abstract":"<p>Amygdalin (AMY), a plant secondary metabolite containing nitrile, is a major component of the seeds of Rosaceae family plants. It is known that this compound has many pharmacological activities such as cancer prevention, antipyretic, and cough suppressant. In this study, the genotoxic and modulatory effects of amygdalin were assessed by chromosomal aberration (CA), sister chromatid exchange (SCE), and cytokinesis-block micronucleus assay (CBMN) assays using human peripheral lymphocytes (HPLs) in the absence and presence of metabolic activator (S9 mix). Lymphocytes were exposed to various concentrations of amygdalin (0.86, 1.72, 3.43, 6.86, and 13.75 μg/mL) alone and in combination with mitomycin-C (MMC, 0.20 μg/mL) or cyclophosphamide (CP, 12 μg/mL). The mitotic index (MI), replication index (RI), cytokinesis-block proliferation index (CBPI), and cytostasis were also evaluated to determine cytotoxicity. Amygdalin alone did not exhibit genotoxic and cytotoxic effects at all the tested concentrations both in the absence and presence of the S9 mix. In contrast, amygdalin significantly reduced the frequencies of CA (especially at 48 h treatments), SCE, and MN (except 0.86 μg/mL in pre- and simultaneous treatment) induced by MMC in all the tested concentrations and treatment protocols. It has also considerably decreased CP-induced CA and SCE frequencies at all the concentrations (except 0.86 μg/mL) in simultaneous treatment. This study demonstrated that amygdalin alone was not genotoxic, on the contrary, it has revealed modulatory effects against chemotherapy agents that induced genomic damage in human lymphocytes, suggesting its chemopreventive potential.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"291-308"},"PeriodicalIF":2.8,"publicationDate":"2023-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10034798","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":"Assessing the quality and making appropriate use of historical negative control data: A report of the International Workshop on Genotoxicity Testing (IWGT).","authors":"Stephen D Dertinger, Dingzhou Li, Carol Beevers, George R Douglas, Robert H Heflich, David P Lovell, Daniel J Roberts, Robert Smith, Yoshifumi Uno, Andrew Williams, Kristine L Witt, Andreas Zeller, Changhui Zhou","doi":"10.1002/em.22541","DOIUrl":"10.1002/em.22541","url":null,"abstract":"<p><p>Historical negative control data (HCD) have played an increasingly important role in interpreting the results of genotoxicity tests. In particular, Organisation for Economic Co-operation and Development (OECD) genetic toxicology test guidelines recommend comparing responses produced by exposure to test substances with the distribution of HCD as one of three criteria for evaluating and interpreting study results (referred to herein as \"Criterion C\"). Because of the potential for inconsistency in how HCD are acquired, maintained, described, and used to interpret genotoxicity testing results, a workgroup of the International Workshops for Genotoxicity Testing was convened to provide recommendations on this crucial topic. The workgroup used example data sets from four in vivo tests, the Pig-a gene mutation assay, the erythrocyte-based micronucleus test, the transgenic rodent gene mutation assay, and the in vivo alkaline comet assay to illustrate how the quality of HCD can be evaluated. In addition, recommendations are offered on appropriate methods for evaluating HCD distributions. Recommendations of the workgroup are: When concurrent negative control data fulfill study acceptability criteria, they represent the most important comparator for judging whether a particular test substance induced a genotoxic effect. HCD can provide useful context for interpreting study results, but this requires supporting evidence that (i) HCD were generated appropriately, and (ii) their quality has been assessed and deemed sufficiently high for this purpose. HCD should be visualized before any study comparisons take place; graph(s) that show the degree to which HCD are stable over time are particularly useful. Qualitative and semi-quantitative assessments of HCD should also be supplemented with quantitative evaluations. Key factors in the assessment of HCD include: (i) the stability of HCD over time, and (ii) the degree to which inter-study variation explains the total variability observed. When animal-to-animal variation is the predominant source of variability, the relationship between responses in the study and an HCD-derived interval or upper bounds value (i.e., OECD Criterion C) can be used with a strong degree of confidence in contextualizing a particular study's results. When inter-study variation is the major source of variability, comparisons between study data and the HCD bounds are less useful, and consequentially, less emphasis should be placed on using HCD to contextualize a particular study's results. The workgroup findings add additional support for the use of HCD for data interpretation; but relative to most current OECD test guidelines, we recommend a more flexible application that takes into consideration HCD quality. The workgroup considered only commonly used in vivo tests, but it anticipates that the same principles will apply to other genotoxicity tests, including many in vitro tests.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2023-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10598234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9874572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotoxicity evaluation of orally administered styrene monomer in mice using comet, micronucleus, and Pig-a endpoints","authors":"B. Bhaskar Gollapudi","doi":"10.1002/em.22540","DOIUrl":"10.1002/em.22540","url":null,"abstract":"<p>Male B6C3F1 mice were administered styrene monomer by oral gavage for 29 consecutive days at dose levels of 0, 75, 150, or 300 mg/kg/day. The highest dose level represented the maximum tolerated dose based on findings in a 28-day dose range-finding study, in which the bioavailability of orally administered styrene was also confirmed. The positive control group received ethyl nitrosourea (ENU; 51.7 mg/kg/day) on Study Days 1–3 and ethyl methanesulfonate (EMS; 150 mg/kg/day) on Study Days 27–29 by oral gavage. Approximately 3 h following the final dose, blood was collected to assess erythrocyte <i>Pig-a</i> mutant and micronucleus frequencies. DNA strand breakage was assessed in glandular stomach, duodenum, kidney, liver, and lung tissues using the alkaline comet assay. The %tail DNA for stomach, liver, lung, and kidney in the comet assay among the styrene-treated groups was neither significantly different from the respective vehicle controls nor was there any dose-related increasing trend in any of the tissues; results for duodenum were interpreted to be inconclusive because of technical issues. The <i>Pig-a</i> and micronucleus frequencies among styrene-treated groups also did not show significant increases relative to the vehicle controls and there was also no evidence for a dose-related increasing trend. Thus, orally administered styrene did not induce DNA damage, mutagenesis, or clastogenesis/aneugenesis in these Organization of Economic Co-operation and Development test guideline-compliant genotoxicity studies. Data from these studies can contribute to the overall assessment of genotoxic hazard and risk posed to humans potentially exposed to styrene.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"282-290"},"PeriodicalIF":2.8,"publicationDate":"2023-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/em.22540","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9681923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of gene expression and inflammation but not DNA damage after sevoflurane anesthesia","authors":"Mariane A. P. Silva,&nbsp;Leandro G. Braz,&nbsp;José Reinaldo C. Braz,&nbsp;Mariana G. Braz","doi":"10.1002/em.22539","DOIUrl":"10.1002/em.22539","url":null,"abstract":"<p>This study assessed, for the first time, the expression of the genes <i>hOGG1</i>, <i>TP53</i>, and <i>IL-6</i> in leukocytes by real-time quantitative polymerase chain reaction in surgical patients before (baseline), during (2 h of anesthesia) and 1 day after sevoflurane anesthesia. Additionally, DNA damage was detected by the comet assay, serum interleukin (IL)-6 was detected by flow cytometry, and differential leukocyte counting was also performed. <i>TP53</i> and <i>hOGG1</i> expression was downregulated on the day after anesthesia compared to before anesthesia. However, <i>IL-6</i> expression did not change, and no DNA damage induction was observed during or after anesthesia. At the systemic level, mild neutrophilia and an increase in IL-6 levels occurred after anesthesia. Our findings suggest that sevoflurane anesthesia downregulates gene expression (<i>hOGG1</i> and <i>TP53</i>) and contributes to an inflammatory status (increased systemic IL-6 and mild neutrophilia) but is not associated with DNA damage in patients without comorbidities who undergo minor elective surgery.</p>","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 5","pages":"315-320"},"PeriodicalIF":2.8,"publicationDate":"2023-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9678356","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":"Letter to “Chepelev et al. Establishing a quantitative framework for regulatory interpretation of genetic toxicity dose–response data: Margin of exposure case study of 48 compounds with both in vivo mutagenicity and carcinogenicity dose–response data”","authors":"Chad M. Thompson,&nbsp;Deborah M. Proctor,&nbsp;Mark A. Harris","doi":"10.1002/em.22537","DOIUrl":"10.1002/em.22537","url":null,"abstract":"To the Editor We read with great interest the recent article by Chepelev et al. (2023) in Environmental and Molecular Mutagenesis. The study expands upon previous important work investigating the relationship between carcinogenic and genotoxic potency of several carcinogens (Soeteman-Hernandez et al., 2016). We were surprised to find sodium dichromate (i.e., hexavalent chromium [Cr(VI)]) among the 48 chemicals investigated by Chepelev et al. despite our previous publication highlighting issues with the inclusion of Cr(VI) in SoetemanHernandez et al. (2016), including the choice of genotoxic endpoint and data indicating that the genotoxic potency of Cr(VI) is likely lower (i.e., higher benchmark dose) than the carcinogenic potency (Thompson et al., 2016). Cr(VI) is a site of contact carcinogen in rodents following oral exposure, inducing tumors in the oral cavity of rats and small intestine of mice (NTP, 2008). Transgenic rodent mutation assays in both rats and mice in target tissues are negative, as are micronucleus assays in the crypts of the mouse small intestine (Thompson et al., 2021). Multiple in vivo blood and bone marrow micronucleus studies in rodents are negative following oral exposure, with the notable exception of results in the am3-C57BL/6 strain of mice (NTP, 2007; Thompson et al., 2021), which SoetemanHernandez et al. (2016) and now Chepelev et al. use as a benchmark for in vivo genotoxic potency of Cr(VI). As discussed in Thompson et al. (2016), we were unable to find any micronucleus studies in am3-C57BL/6 mice aside from Cr(VI) thereby calling into question the validity of using results from this strain as a benchmark for the genotoxic potency of Cr(VI), especially when there are several negative in vivo micronucleus assays (Thompson et al., 2021). Notably, NTP (2007) reported only the combined results of two am3-C57BL/6 assays as positive, even though their website indicates that one study was negative. Soeteman-Hernandez et al. (2016) and Chepelev et al. appear to have only modeled the positive am3-C57BL/6 assay. Moreover, in vivo genotoxicity data published before 2016 and since indicate that the tumors in NTP (2008) are not the result of a genotoxic mode of action (Thompson et al., 2021), but rather sustained intestinal injury in mice (Bhat et al., 2020) and unknown mechanisms in rats. Chepelev et al. also highlight Cr(VI) as having margin of exposure (MOE) values ≤10,000; however, the exposure estimate the authors used was conservatively set to 0.1 mg/kg/day due to the supposed lack of exposure data. However, most chromium in biota is likely trivalent chromium due to the presence of reducing agents in gastric fluid and cells. Most chromium in groundwater sources is Cr(VI) (Seidel & Corwin, 2013) and US Environmental Protection Agency's (EPA) own environmental monitoring data indicate median and 95th percentile Cr(VI) levels of 0.001 and 0.003 ppm, respectively, resulting in daily exposures on the order of 3E-5 to 9E-5 mg/kg","PeriodicalId":11791,"journal":{"name":"Environmental and Molecular Mutagenesis","volume":"64 4","pages":"259-260"},"PeriodicalIF":2.8,"publicationDate":"2023-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/em.22537","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9735752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}