Mutation research. Genetic toxicology and environmental mutagenesis最新文献_第4页

Effect of xthA deletion in the activation of the E. coli SOS response by gamma rays, UV-C light and other genotoxic agents xthA缺失对γ射线、UV-C光和其他基因毒性物质激活大肠杆菌SOS反应的影响

IF 2.5 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-08-01 Epub Date: 2025-08-05 DOI: 10.1016/j.mrgentox.2025.503879

Jorge Serment-Guerrero , Viridiana Dominguez-Monroy , Martha Patricia Cruces-Martinez , Jorge Luis Fuentes-Lorenzo , Silvia Cristina Serment-Gonzalez

The SOS response contains a set of about 45 genes related to the repair or tolerance to DNA damage. These genes are normally blocked but when lesions upon the genetic material occur an SOS signal is generated allowing their expression. Most types of DNA lesions must be modified or processed to induce SOS. In a previous work, a model was proposed suggesting the possible paths that could be followed from the different types of lesions to the induction of the response. One of these possible routes is through the base excision repair mechanism (BER). Since in E. coli the AP endonuclease exonuclease III plays a key role in this repair pathway, in the present study we evaluate the participation of xthA product in the processing of DNA lesions made by gamma rays, UV-C light, ethyl methanesulphonate, methyl methanesulphonate, mitomycin C, hydrogen peroxide and tert-buthylhydroperoxide to trigger the SOS response. A strain defective in xthA and a wt strain were exposed to different genotoxic agents and survival and SOS induction were analyzed. The results show differences in the survival and SOS induction to each genotoxic agent between the wt strain and the xthA mutant; depending on the type of DNA damage inflicted, the SOS response level was either higher or lower compared to the wt strain. This suggests that while the AP endonuclease role of exonuclease III enzyme suppresses SOS induction when bulky and methylated lesions occur, it enhances SOS induction when the damage is generated by ROS, in agreement with a previously proposed model.

SOS反应包含一组约45个基因，这些基因与DNA损伤的修复或耐受有关。这些基因通常是被阻断的，但当遗传物质发生病变时，就会产生SOS信号，允许它们表达。大多数类型的DNA损伤必须经过修饰或处理才能诱发SOS。在之前的工作中，提出了一个模型，提出了从不同类型的病变到诱导反应的可能路径。其中一个可能的途径是通过碱基切除修复机制（BER）。由于在大肠杆菌中，AP核酸内切酶外切酶III在这一修复途径中起着关键作用，因此在本研究中，我们评估了xthA产物在伽马射线、UV-C光、甲磺酸乙酯、甲磺酸甲酯、丝裂霉素C、过氧化氢和过氧化叔丁基氢引起的DNA损伤的处理中参与SOS反应。将一株xthA缺陷菌株和一株wt菌株暴露于不同的基因毒性物质中，分析其存活和SOS诱导情况。结果表明，wt菌株和xthA突变体的存活率和对各基因毒性物质的SOS诱导存在差异；根据DNA损伤类型的不同，与wt菌株相比，SOS反应水平或高或低。这表明，虽然外切酶III酶的AP内切酶作用在大体积和甲基化病变发生时抑制SOS诱导，但当ROS产生损伤时，它会增强SOS诱导，这与先前提出的模型一致。

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引用次数: 0

Epistatic interactions in DNA repair genes as biomarkers of susceptibility for DNA damage in pesticide-exposed agricultural workers of Punjab, North-West India DNA修复基因的上位相互作用作为农药暴露农业工人DNA损伤易感性的生物标志物

IF 2.5 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-08-01 Epub Date: 2025-07-30 DOI: 10.1016/j.mrgentox.2025.503880

Karashdeep Kaur , Rupinder Kaur

Some occupational exposures to pesticides have been associated with genotoxicity which arises from DNA single-strand breaks (SSBs), repair of DNA double-strand breaks (DSBs), DNA adduct formation, or DNA-DNA and DNA-protein cross-links. Polymorphisms in genes encoding enzymes of DNA repair pathways may modulate the individual’s susceptibility to pesticide-induced genotoxicity. A total of 450 subjects were included in this study, which comprises 225 agricultural workers exposed to complex mixtures of pesticides and 225 non-exposed controls from Punjab, North-West India. Susceptibility of OGG1 Ser326Cys (C1245G), XRCC1 Arg194Trp (C26304T), XRCC1 Arg399Gln (G28152A), XPC Lys939Gln (A2920C), XPC Ala499Val (C21151T), XPD Asp312Asn (G23591A), XPD Lys715Gln (A35931C), XPF Arg415Gln (G1244A), XPG Asp1104His (G3507C), ERCC1 3′-UTR (C8092A) and ERCC1 Asn118Asn (C354T) gene polymorphisms with pesticide-induced DNA damage was determined by Kruskal-Wallis test. The association of epistatic gene interactions with DNA damage was studied by ANOVA. The results indicated significant interactions of variant OGG1 326Ser/Cys genotype with XRCC1 194Arg/Trp and XRCC1 399Arg/Gln genotypes in increased susceptibility to DNA damage. XPC 939Gln/Gln genotype significantly interacts with XPC 499Ala/Val, XPD 312Asp/Asp and XPD 715Gln/Gln variant genotypes to increase DNA damage susceptibility. Among exposed XPF 415Gln/Gln individuals, DNA damage was significantly higher in those individuals who had variant XPG Asp/His and ERCC1 8092CA genotypes. We observed some statistically significant epistatic gene interactions in DNA repair pathways in modulating DNA damage, which may be used as biomarkers of susceptibility in pesticide-exposed agricultural workers of Punjab, North-West India.

一些职业性农药暴露与DNA单链断裂（SSBs）、DNA双链断裂（DSBs）修复、DNA加合物形成或DNA-DNA和DNA-蛋白质交联引起的遗传毒性有关。编码DNA修复途径酶的基因多态性可能调节个体对农药遗传毒性的易感性。本研究共纳入450名受试者，其中包括225名接触复杂农药混合物的农业工人和225名来自印度西北部旁遮普省的非接触对照者。采用Kruskal-Wallis试验检测OGG1 Ser326Cys （C1245G）、XRCC1 Arg194Trp （C26304T）、XRCC1 Arg399Gln （G28152A）、XPC Lys939Gln （A2920C）、XPC Ala499Val （C21151T）、XPD Asp312Asn （G23591A）、XPD Lys715Gln （A35931C）、XPF Arg415Gln （G1244A）、XPG Asp1104His （G3507C）、ERCC1 Asn118Asn （C354T）基因多态性与农药诱导DNA损伤的易感性。通过方差分析研究上位性基因相互作用与DNA损伤的关系。结果表明，变异OGG1 326Ser/Cys基因型与XRCC1 194Arg/Trp和XRCC1 399Arg/Gln基因型的交互作用显著增加了DNA损伤的易感性。XPC 939Gln/Gln基因型与XPC 499Ala/Val、XPD 312Asp/Asp和XPD 715Gln/Gln基因型显著相互作用，增加DNA损伤易感性。在暴露的XPF 415Gln/Gln个体中，变异XPG Asp/His和ERCC1 8092CA基因型个体的DNA损伤显著更高。我们观察到在DNA修复途径中调节DNA损伤的一些具有统计学意义的epistatic基因相互作用，这可能被用作印度西北部旁遮普省农药暴露农业工人的易感性生物标志物。

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引用次数: 0

Radiology personnel chronically exposed to low-dose ionizing radiation: Assessment of genotoxic damage with the buccal micronucleus cytome assay 长期暴露于低剂量电离辐射的放射学人员：用口腔微核细胞组测定法评估遗传毒性损伤

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-07-01 Epub Date: 2025-06-12 DOI: 10.1016/j.mrgentox.2025.503872

Serap Yüce Emiroğlu , Tülay Aşkın Çeli̇k

Objective

This study aimed to assess the genotoxic effects of chronic occupational exposure to low-dose ionizing radiation among healthcare professionals employed at three hospitals in Aydın, Turkey: Aydın Adnan Menderes University Research and Application Hospital (ADU-UAH), Atatürk State Hospital, and Aydın State Hospital. The exposed group comprised 27 healthcare workers routinely operating in radiation-related departments, while 27 matched individuals with no known exposure constituted the control group.

Methods

Genetic damage was evaluated using the exfoliated buccal micronucleus cytome (BMCyt) assay, a validated and non-invasive method for human biomonitoring. Frequencies of nuclear abnormalities—including micronuclei, binucleated cells, nuclear buds, condensed chromatin, karyorrhexis, karyolysis, and pyknotic cells—were systematically recorded and compared between groups.

Results

A statistically significant increase in all genotoxic markers was observed in the exposed group compared to controls (p < 0.05). The highest frequency of micronucleated cells was found in workers at Aydın State Hospital (32.38 ‰), approximately 30-fold higher than the control group (2.84 ‰). Healthcare workers at ADU-UAH and Atatürk State Hospital exhibited moderate yet notable elevations, with frequencies of 24.85 ‰ and 17.28 ‰, respectively. Sex-stratified analysis revealed minor but statistically significant differences, with male workers showing slightly higher genotoxicity levels (p < 0.05), although female staff exhibited higher nuclear anomalies at certain institutions.

Conclusion

Our findings indicate that chronic exposure to low-dose ionizing radiation is associated with increased genomic instability among healthcare workers. The elevated frequency of nuclear abnormalities highlights a potential long-term mutagenic risk in occupational settings. These results underscore the urgent need for reinforced radiation safety protocols, routine biomonitoring, and institutional policy revisions to mitigate genotoxic risks. Further studies are warranted to elucidate the mechanisms underlying radiation-induced genomic damage and to better understand individual susceptibility patterns in exposed populations.

目的本研究旨在评估土耳其Aydın三家医院（Aydın Adnan Menderes大学研究与应用医院（ADU-UAH）、atatrk国立医院和Aydın国立医院）的医疗保健专业人员慢性职业暴露于低剂量电离辐射的遗传毒性效应。受照组由27名在辐射相关部门常规工作的医护人员组成，而27名没有已知受照的匹配个体组成对照组。方法采用脱落颊微核细胞组（BMCyt）测定法对遗传损伤进行评估，BMCyt是一种经过验证的无创人体生物监测方法。系统记录核异常的频率，包括微核、双核细胞、核芽、浓缩染色质、核分裂、核溶解和固缩细胞，并比较各组之间的差异。结果暴露组各基因毒性指标均较对照组升高，差异有统计学意义（p <； 0.05）。微核细胞出现频率最高的是Aydın国立医院的工人（32.38 ‰），约为对照组（2.84 ‰）的30倍。ADU-UAH和atatatrk州立医院的医护人员表现出中度但显著的升高，频率分别为24.85 ‰和17.28 ‰。性别分层分析显示了微小但具有统计学意义的差异，男性工人的遗传毒性水平略高（p <； 0.05），尽管某些机构的女性员工表现出更高的核异常。结论：我们的研究结果表明，长期暴露于低剂量电离辐射与医护人员基因组不稳定性增加有关。核异常频率的升高突出了职业环境中潜在的长期诱变风险。这些结果强调迫切需要加强辐射安全协议，常规生物监测和制度政策修订，以减轻遗传毒性风险。需要进一步的研究来阐明辐射引起的基因组损伤的机制，并更好地了解暴露人群的个体易感性模式。

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引用次数: 0

Photogenotoxicity of N-nitrosoproline plus simultaneous UVA irradiation in human-derived keratinocytes n-亚硝基脯氨酸加同时UVA照射对人源性角质形成细胞的光毒性

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-07-01 Epub Date: 2025-07-13 DOI: 10.1016/j.mrgentox.2025.503876

Naomi Tomozane , Noriko Tanaka , Sakae Arimoto-Kobayashi

In this study, we investigated the genotoxicity of N-nitrosoproline (NPRO) in human-derived keratinocytes (HaCaT and NCTC2544 cells) using simultaneous UVA irradiation without metabolic activation. NPRO plus UVA exhibited dose- and intensity-dependent micronuclei formation in the keratinocytes, as well as nitric oxide (NO) production. The action spectra of genotoxicity and NO formation from NPRO plus UVA followed the absorption curve of NPRO, indicating that photoenergy was absorbed by the NPRO-triggered photoreaction. A significant increase in cyclic guanosine monophosphate (cGMP) was observed in HaCaT cells treated with NPRO plus UVA. NO production from UVA-irradiated NPRO paralleled micronuclei formation, and the phototoxicity of NPRO may have simultaneously interfered with the cGMP-related signaling systems caused by NO from photoactivated NPRO.

在这项研究中，我们研究了n-亚硝基脯氨酸（NPRO）在无代谢激活的同时UVA照射下对人源性角质形成细胞（HaCaT和NCTC2544细胞）的遗传毒性。NPRO加UVA在角质形成细胞中表现出剂量和强度依赖的微核形成，以及一氧化氮（NO）的产生。NPRO + UVA的遗传毒性和生成NO的作用谱符合NPRO的吸收曲线，说明NPRO触发的光反应吸收了光能。在NPRO加UVA处理的HaCaT细胞中，cGMP显著增加。uva辐照NPRO产生的NO与微核形成平行，NPRO的光毒性可能同时干扰了NPRO光活化NO引起的cgmp相关信号系统。

引用次数: 0

Significant new developments in genetic toxicology testing 遗传毒理学检测的重大新进展

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-07-01 Epub Date: 2025-06-11 DOI: 10.1016/j.mrgentox.2025.503873

Miroslav Mišík, P. David Josephy, Helga Stopper, Siegfried Knasmueller

引用次数: 0

Bleomycin induces short-term telomere fragility in Epstein-Barr virus-transformed human lymphoblastoid cells 博莱霉素诱导Epstein-Barr病毒转化的人淋巴母细胞的短期端粒脆性

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-07-01 Epub Date: 2025-07-16 DOI: 10.1016/j.mrgentox.2025.503877

Andrea G. Cardozo , Daniel C. Castrogiovanni , Julieta M. Parisi , Alejandro D. Bolzán

The induction of telomere dysfunction-related chromosomal aberrations by the radiomimetic antibiotic bleomycin (BLM) was studied in human lymphoblastoid cells immortalized with the Epstein-Barr virus (EBV). To this end, an EBV-induced lymphoblastoid cell line (T-37) was exposed to increased concentrations of BLM (10–100 µg/mL) for 2 h at 37ºC, and telomere aberrations were analyzed 24 h (first mitosis) after treatment using PNA-FISH with pan-telomeric plus pan-centromeric probes. Telomere signal duplications (TSD) increased significantly in BLM-exposed cells (p < 0.01), although the concentration-response relationship was non-linear. Most of the induced TSD (95–99 %) were of chromatid-type. No induction of telomere signal loss, telomere fusions or telomere associations by BLM was observed in T-37 cells. These findings show that BLM induces short-term telomere dysfunction in EBV-transformed human lymphoblastoid cells in the form of TSD (which implies telomere fragility) and suggest that these effects mainly occur during the G2 stage of the cell cycle. The persistence of this type of aberrations in the long-term in EBV-induced lymphoblastoid cells and other human cells exposed to BLM may be of medical relevance. Telomere fragility induced by BLM could promote genomic instability, which might contribute to the development of secondary tumors in patients undergoing chemotherapy based on this compound. Consequently, our study raises concerns about the potential long-term genomic effects of BLM in treated patients and suggests that the analysis of TSD could be a useful biomarker for detecting BLM-induced telomere dysfunction in human cells.

在用eb病毒（EBV）永生化的人淋巴母细胞样细胞中，研究了拟放射抗生素博来霉素（BLM）诱导端粒功能障碍相关染色体畸变的作用。为此，将ebv诱导的淋巴母细胞样细胞系（T-37）在37℃下暴露于浓度增加的BLM（10-100µg/mL）中2 h，并在处理后24 h（第一次有丝分裂）使用带有泛端粒和泛着丝粒探针的PNA-FISH分析端粒畸变。在blm暴露的细胞中，端粒信号重复（TSD）显著增加（p <； 0.01），尽管浓度-响应关系是非线性的。大多数诱导的TSD（95% ~ 99%）为染色单体型。在T-37细胞中未观察到BLM诱导端粒信号丢失、端粒融合或端粒关联。这些发现表明，BLM在ebv转化的人淋巴母细胞样细胞中以TSD的形式诱导短期端粒功能障碍（这意味着端粒脆弱），并表明这些影响主要发生在细胞周期的G2阶段。在eb病毒诱导的淋巴母细胞样细胞和其他暴露于BLM的人类细胞中，这种类型的畸变长期持续存在可能具有医学意义。BLM诱导的端粒脆性可促进基因组不稳定性，这可能导致基于该化合物的化疗患者继发性肿瘤的发展。因此，我们的研究引起了对BLM对治疗患者潜在的长期基因组影响的关注，并表明对TSD的分析可能是检测BLM诱导的人类细胞端粒功能障碍的有用生物标志物。

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引用次数: 0

Genome-wide mutation analysis induced by mutagens in TK6 cells using Hawk-Seq™ 利用Hawk-Seq™对诱变剂诱导的TK6细胞全基因组突变进行分析

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-07-01 Epub Date: 2025-07-12 DOI: 10.1016/j.mrgentox.2025.503875

Yuki Otsubo , Takako Hirose , Shoji Matsumura , Sayaka Hosoi , Kazutoshi Saito , Masaaki Miyazawa

Error-corrected next-generation sequencing (ecNGS) sensitively detects rare mutations in biological models. We applied Hawk-Seq™ to evaluate chemical-induced mutations using the IVGT TK6 human lymphoblastoid cell line. Since clonal and sub-clonal variants (CVs and SCVs) decrease mutation detection sensitivity, we first identified 4,501,430 CVs compared to GRCh38 by resequencing the TK6 genome. The overall base substitution (BS) frequency in vehicle controls after filtering out these variants was 2.0 × 10⁻⁶ base pairs (bp), relatively higher than in other ecNGS studies. A total of 4974 sites provided the same types of BSs in ≥ 2 vehicle controls, suggesting that SCVs increased the error frequency. After filtering out these sites, the overall background BS frequency significantly decreased (0.93 × 10⁻⁶ bp). Therefore, we filtered out the potential SCV positions identified using resequencing data with increased depth (mean depth of ca. 110), reducing the background overall BS frequency to 0.65 × 10⁻⁶ bp. Finally, we evaluated DNA samples from TK6 cells exposed to N-methyl-N-nitrosourea (MNU) and N-ethyl-N-nitrosourea (ENU) for 24 h. The overall BS frequencies in MNU- and ENU-treated samples were 9.0 × 10⁻⁶ and 2.0 × 10⁻⁶ bp, respectively, significantly improving the signal-to-noise ratio. MNU predominantly induced G:C > A:T (21 × 10⁻⁶ bp), 62 times higher than that induced by vehicle controls. ENU primarily induced G:C > A:T (2.7 × 10⁻⁶ bp) and significantly increased A:T > C:G and A:T > G:C frequencies (∼10⁻⁷ bp). Our method sensitively detected mutations, including minor patterns, indicating its potential to reflect various mutagenic mechanisms.

错误校正的下一代测序（ecNGS）可以灵敏地检测生物模型中的罕见突变。我们使用Hawk-Seq™来评估IVGT TK6人淋巴母细胞样细胞系的化学诱导突变。由于克隆和亚克隆变异（CVs和scv）降低了突变检测的敏感性，我们首先通过对TK6基因组进行重测序，鉴定出与GRCh38相比的4,501,430个CVs。在滤除这些变异后，车辆对照的总体碱基替换（BS）频率为2.0 × 10−6碱基对（bp），相对高于其他ecNGS研究。在≥ 2个载体对照中，共有4974个位点提供了相同类型的BSs，这表明scv增加了错误频率。过滤这些位点后，总体背景BS频率显著降低（0.93 × 10−6 bp）。因此，我们通过增加深度（平均深度约为110）的重测序数据过滤出潜在的SCV位置，将背景总BS频率降低到0.65 × 10−6 bp。最后，我们评估了暴露于n -甲基-n -亚硝基脲（MNU）和n -乙基-n -亚硝基脲（ENU） 24 h的TK6细胞的DNA样本。MNU和enu处理后样品的总BS频率分别为9.0 × 10−6 bp和2.0 × 10−6 bp，显著提高了信噪比。MNU主要诱导G:C >； A:T(21 × 10−6 bp)，比对照高62倍。ENU主要诱导G:C >； A:T频率（2.7 × 10−6 bp），显著增加A:T >； C:G和A:T >； G:C频率（~ 10−7 bp）。我们的方法灵敏地检测突变，包括次要模式，表明其反映各种致突变机制的潜力。

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引用次数: 0

Low-dose bisphenol A plus arsenite: Continuous or intermittent exposures in Sprague-Dawley rats; Effects on kidney oxidative stress, DNA damage, ferroptosis, and fibrosis 低剂量双酚A加亚砷酸盐：Sprague-Dawley大鼠连续或间歇暴露对肾脏氧化应激、DNA损伤、铁下垂和纤维化的影响

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-05-01 Epub Date: 2025-04-26 DOI: 10.1016/j.mrgentox.2025.503871

Girija Prasanna Sahoo, Asutosh Pattnaik, Vinod Kumar, Gopabandhu Jena

Arsenic and bisphenol A (BPA) are widespread environmental pollutants. We have studied the nephrotoxicity of arsenite (ARS), 10 mg/L in drinking water, plus BPA, 50 µg/kg oral dose, in juvenile Sprague-Dawley rats. Animals were randomized into seven groups and exposed to the chemicals either continuously or intermittently, for 8 weeks. The parameters evaluated were urine biomarkers, histopathological and transmission electron microscopic (TEM) examinations, DNA damage (halo assay), and protein expressions. Continuous exposure to AS and BPA significantly increased urinary creatinine, albumin, and total protein, and decreased blood urea nitrogen (BUN). Histopathological and TEM data showed brush border detachment, iron accumulation, podocyte injury, increased slit diaphragm space, and collagen deposition in both exposure groups. Significantly greater DNA damage was seen in the combined-exposure group than in the other experimental groups. Combination exposure in the continuous and intermittent groups showed renal fibrosis and ferroptosis and gene expression analysis revealed a significant increase in Bax and decrease in SIRT 1. Combination exposure was more harmful than the individual exposures in causing kidney injury in these animals.

砷和双酚A （BPA）是广泛存在的环境污染物。我们研究了饮用水中10 mg/L亚砷酸盐（ARS）加50µg/kg口服剂量BPA对幼年Sprague-Dawley大鼠的肾毒性。动物被随机分为七组，连续或间歇地暴露在化学物质中，持续8周。评估的参数包括尿液生物标志物、组织病理学和透射电子显微镜（TEM）检查、DNA损伤（光晕测定）和蛋白质表达。持续暴露于AS和BPA显著增加尿肌酐、白蛋白和总蛋白，降低血尿素氮（BUN）。组织病理学和透射电镜数据显示，在两个暴露组中，刷状边界脱落、铁积累、足细胞损伤、狭缝隔膜间隙增加和胶原沉积。与其他实验组相比，联合暴露组的DNA损伤明显更大。连续组和间歇组的联合暴露显示肾纤维化和铁上吊，基因表达分析显示Bax显著升高，sirt1显著降低。联合暴露比单独暴露对肾损伤的危害更大。

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引用次数: 0

DNA damage and oxidative stress responses to pollution of Mytilus galloprovincialis L. from the Izmir Bay (Turkey): Seasonal evaluation 土耳其伊兹密尔湾贻贝（Mytilus galloprovincialis L.）对污染的DNA损伤和氧化应激反应：季节评价

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-05-01 Epub Date: 2025-03-23 DOI: 10.1016/j.mrgentox.2025.503866

Ebru Yayla , Cem Guler , Aylin Buhur , Nefise Ulku Karabay Yavasoglu , Selma Katalay , Cinel Koksal Karayildirim

In the current study, the relationship between DNA damage and heavy metal pollutions was evaluated by sampling mussels from Izmir Bay (Turkey), which has different anthropogenic impacts in the Aegean Sea. M. galloprovincialis was selected as a bioindicator organism to determine the heavy metal amounts, SOD, CAT, TBARS levels and to detect the DNA damage in 4 different stations of Izmir Bay. A significant increase was detected in all heavy metals in the digestive gland tissue of the mussels collected from the Alsancak in summer compared to spring. Especially, Zn levels of gills and digestive glands of mussels collected from Alsancak in summer were detected 22.411 and 40.447 μg/g, respectively. According to MPI values, significant differences were determined in Urla and the highest accumulation was calculated in gill tissue. The activities of SOD and CAT enzymes were found at a very high level in mussel gills and glands at all stations except Urla in summer compared to them in spring. Additionally, TBARS levels were higher in mussel gills and gonad tissues at Inciralti and Urla stations in summer compared to spring samples. DNA damage classification in mussel hemocytes from all stations was identified according to the Comet assay. The test results showed that a statistically significant decrease in DNA% in comet tails in hemocytes of mussels collected from all stations in Summer was found compared to them in Spring. Also, at all stations except Alsancak, the genetic damage index decreased in summer compared to spring. While a positive correlation was detected between heavy metal pollution and DNA damage in mussels taken from Alsancak and Inciraltı (r = 0.734), a significant correlation was detected in Pasaport and Urla in both seasons (r = 0.999). This study indicates that heavy metal contaminations in the mussels of Izmir Bay are still an environmental problem on this area. DNA damage is an appropriate biomarker for genotoxicity evaluation even in low heavy metal contaminated areas.

本研究通过对爱琴海受到不同人为影响的土耳其伊兹密尔湾贻贝取样，评估了DNA损伤与重金属污染之间的关系。在伊兹密尔湾4个不同监测站，选取加洛毛霉作为生物指示生物，测定土壤重金属含量、SOD、CAT、TBARS水平及DNA损伤检测。与春季相比，夏季在阿尔桑卡克采集的贻贝的消化腺组织中检测到的所有重金属都显着增加。其中，夏季采集的贻贝鳃和消化腺锌含量分别为22.411和40.447 μg/g。根据MPI值，确定了Urla的显著差异，并计算了鳃组织的最高蓄积量。除乌拉市外，夏季各试验点贻贝鳃和腺体SOD和CAT酶活性均高于春季。此外，与春季样本相比，夏季Inciralti和Urla站贻贝鳃和性腺组织中的TBARS水平较高。所有站点贻贝血细胞的DNA损伤分类根据Comet测定法确定。结果表明，夏季采集贻贝血细胞中彗尾DNA含量较春季显著降低。此外，除Alsancak外，所有站点的遗传损害指数在夏季都比春季下降。在Alsancak和inciralti采集的贻贝中，重金属污染与DNA损伤呈正相关（r = 0.734），而在Pasaport和Urla采集的贻贝中，两个季节重金属污染与DNA损伤呈显著相关（r = 0.999）。该研究表明，伊兹密尔湾贻贝重金属污染仍然是该地区的环境问题。即使在低重金属污染地区，DNA损伤也是一种适宜的遗传毒性评价生物标志物。

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引用次数: 0

A study of radiation workers: Dosimetry, chromosomal aberrations, and cancer risk 辐射工作人员的研究：剂量学、染色体畸变和癌症风险

IF 2.3 4区医学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation research. Genetic toxicology and environmental mutagenesis

Pub Date : 2025-05-01 Epub Date: 2025-04-12 DOI: 10.1016/j.mrgentox.2025.503869

Gyöngyi Farkas , Réka Király , Gábor Székely , Zsuzsa S. Kocsis , Gyöngyvér Orsolya Sándor , Csilla Pesznyák , Tibor Major , Zoltán-Takácsi Nagy , Zsolt Jurányi

Cytogenetic analysis of blood lymphocytes can be used as a biomarker of absorbed radiation dose. The frequency of chromosomal aberrations (CA) correlates with subsequent cancer incidence. Healthy medical employees in Hungary - 301 working in an ionizing radiation work area and 732 controls - were studied from 1997 to 2022. Frequencies of chromatid- and chromosome-type aberrations in peripheral blood lymphocytes were significantly higher in the ionizing radiation group. Smoking also affected the frequency of aberrations, which was highest among smokers in the radiation group. Staff working with ionizing radiation were divided into four groups: CT, radiation therapy, diagnostic X-ray, and nuclear medicine. Total aberrations and aberrant cells were significantly higher in the nuclear medicine group than in the CT group. Tumor cases were not more frequent among the ionizing radiation group than among the control group.

血液淋巴细胞的细胞遗传学分析可作为辐射吸收剂量的生物标志物。染色体畸变（CA）的频率与随后的癌症发病率相关。从1997年到2022年，对匈牙利的健康医务人员进行了研究，其中301人在电离辐射工作区域工作，732人作为对照。电离辐射组外周血淋巴细胞染色单体和染色体型畸变频率明显升高。吸烟也影响了畸变的频率，在接受辐射的那组吸烟者中，畸变的频率最高。从事电离辐射工作的工作人员被分为四组：CT组、放射治疗组、诊断x线组和核医学组。核医学组总畸变数及畸变细胞数明显高于CT组。电离辐射组的肿瘤病例并不比对照组多。

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