Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Pesticide exposure and oxidative stress generation are linked to poor prognosis outcomes in breast cancer women carrying the allelic variant rs7438135 in the UGT2B7 gene","authors":"Beatriz Geovana Leite Vacario,&nbsp;Isabely Mayara da Silva,&nbsp;Murilo Galvani Machado,&nbsp;Julia Fernandes Gois Orrutéa,&nbsp;Aline Graciele Henriques Campos,&nbsp;Rafaela Oliveira Matos,&nbsp;Ana Carolina Lopes Federige,&nbsp;Bruna Yukie Koizumi,&nbsp;Maikely Bruna Leite,&nbsp;Isabela Mitsu Suo Komori,&nbsp;Hellen dos Santos Jaques,&nbsp;Daniel Rech,&nbsp;Roberta Losi Guembarovski,&nbsp;Marla Karine Amarante,&nbsp;Juliana Mara Serpeloni,&nbsp;Carolina Panis","doi":"10.1002/jbt.70013","DOIUrl":"10.1002/jbt.70013","url":null,"abstract":"<p>Pesticide exposure is a risk factor for the development of several diseases, including breast cancer (BC). The enzyme <i>UGT2B7</i> participate in detoxification of pesticides and the presence rs7438135 (G &gt; A) variant in your gene increases its glucuronidation potential, contributing to oxidative stress metabolites neutralization. Here we investigated the impact of occupational pesticide exposure on the systemic oxidative stress generation from 228 women with BC depending on their UGT2B7 rs7438135 (G &gt; A) status. q-PCR investigated the presence of the rs7438135 variant, and oxidative stress markers (lipid peroxidation levels, total antioxidant capacity—TRAP, and nitric oxide metabolites—NOx) were measured in plasma. Pesticide exposure induced significant augment in the systemic lipid peroxidation in the presence of the variant for several clinicopathological conditions, including tumors with high proliferation index (ki67) and with high aggressiveness. NOx was augmented in high ki67, positive progesterone receptors, high-grade and triple-negative/Luminal B tumors, and low-risk stratified patients. TRAP was depleted in young patients at menopause and those with triple-negative/Luminal B tumors, as well as those stratified as at low risk for death and recurrence. These findings showed that the presence of the variant was not able to protect from pesticide-induced oxidative stress generation in BC patients.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to “the Letter to the Editor by Yoshida et al., Monosodium glutamate added to food does not induce damage to the pancreas nor aggravate diabetes due to enhancement of oxidative stress” for editorial evaluation","authors":"Sevda Urcar Gelen","doi":"10.1002/jbt.23860","DOIUrl":"10.1002/jbt.23860","url":null,"abstract":"","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to RETRACTION: Protective effects of caffeic acid on lactate dehydrogenase isoenzymes, electrocardiogram, adenosine triphosphatases, and hematology on Isoproterenol-Induced myocardial infarcted rats","authors":"","doi":"10.1002/jbt.23867","DOIUrl":"10.1002/jbt.23867","url":null,"abstract":"<p>“RETRACTION: Protective Effects of Caffeic Acid on Lactate Dehydrogenase Isoenzymes, Electrocardiogram, Adenosine Triphosphatases, and Hematology on Isoproterenol-Induced Myocardial Infarcted Rats,” <i>Journal of Biochemical and Molecular Toxicology</i> 38, no. 10 (2024): e23858, https://doi.org/10.1002/jbt.23858.</p><p>In the previously published retraction note, the reasons for the retraction were described inaccurately and the authors' disapproval of the retraction was not reflected. This has now been addressed and corrected below.</p><p>The retraction has been agreed following an investigation into concerns raised by a third party, which revealed that some of the bands presented in the agarose gel electrophoresis in Figure 1 have been published in another article by one of the same authors. The gels in the two articles represent different experiments. The authors did not provide a satisfactory explanation or their original data. The editors consider the results and conclusion reported in this article unreliable. The authors disagree with the retraction.</p><p>We apologize for this error.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.23867","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Enhanced Chemotherapeutic Efficacy of Docetaxel in Human Lung Cancer Cell Line via GLUT1 Inhibitor","authors":"","doi":"10.1002/jbt.23865","DOIUrl":"10.1002/jbt.23865","url":null,"abstract":"<p><b>RETRACTION:</b> M. Bahremani, N. Rashtchizadeh, M. Sabzichi, A. M. Vatankhah, S. Danaiyan, H. Poursistany, J. Mohammadian, and A. Ghorbanihaghjo, “Enhanced Chemotherapeutic Efficacy of Docetaxel in Human Lung Cancer Cell Line via GLUT1 Inhibitor,” <i>Journal of Biochemical and Molecular Toxicology</i> 37, no. 6 (2023): e23348, https://doi.org/10.1002/jbt.23348.</p><p>The above article, published online on 31 March 2023 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Hari K. Bhat; and Wiley Periodicals, LLC. The retraction has been agreed due to concerns raised by a third party on the data presented in the article. Specifically, some image elements in Figure 5 were found to have been published elsewhere in a different scientific context. Raw data for the replicate experiments related to Figure 5 were provided by the corresponding author Jamal Mohammadian upon request. The data received raised further concerns, as additional overlap with previously published sources was detected. Despite the authors performed a new experiment to replicate the findings of the originally published Figure 5, the article is retracted as the editors have lost trust in the accuracy and integrity of the full body of data presented in the article and consider its conclusions invalid. The corresponding author Jamal Mohammadian disagrees with the decision of retraction. No confirmation was obtained by the remaining co-authors.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.23865","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the interplay of PPAR gamma inhibition and energy demand in adriamycin-induced cardiomyopathy: In Vitro and In Vivo perspective","authors":"Kalaiselvi Seenivasan,&nbsp;Sankarganesh Arunachalam,&nbsp;Tirupathi Pichiah P. B.,&nbsp;Sanjay B. Vasan,&nbsp;Meenakshi R. Venkateswaran,&nbsp;Durairaj Siva,&nbsp;Jeeva Gothandam,&nbsp;Shanmugam Achiraman","doi":"10.1002/jbt.23855","DOIUrl":"https://doi.org/10.1002/jbt.23855","url":null,"abstract":"<p>Adriamycin is an anticancer anthracycline drug that inhibits the progression of topoisomerase II activity and causes apoptosis. The effective clinical application of the drug is very much limited by its adverse drug reactions on various tissues. Most importantly, Adriamycin causes cardiomyopathy, one of the life-threatening complications of the drug. Altered expression of PPARγ in adipocytes inhibited the glucose and fatty acids uptake by down regulating GLUT4 and CD36 expression and causes cardiotoxicity. Therefore, the influence of Adriamycin in cardiac ailments was investigated in vivo and in vitro. Adriamycin treated rats showed altered ECG profile, arrhythmic heartbeat with the elevated levels of CRP and LDH. Dysregulated lipid profiles with elevated levels of cholesterol and triglycerides were also observed. Possibilities of cardiac problems due to cardiomyopathy were analyzed through histopathology. Adriamycin treated rats showed no signs for atheromatous plaque formation in aorta but disorganized cardiomyocytes with myofibrillar loss and inflammation in heart tissue, indicative of cardiomyopathy. Reduced levels of antioxidant enzymes confirmed the incidence of oxidative stress. Adriamycin treatment significantly reduced glucose and insulin levels, creating energy demand due to decreased glucose and insulin levels with increased fatty acid accumulation, ultimately resulting in oxidative stress mediated cardiomyopathy. Since PPARs play a vital role in regulating oxidative stress, the effect of Adriamycin on PPARγ was analyzed by western blot. Adriamycin downregulated PPARγ in a dose-dependent manner in H9C2 cells in vitro. Overall, our study suggests that Adriamycin alters glucose and lipid metabolism via PPARγ inhibition that leads to oxidative stress and cardiomyopathy that necessitates a different therapeutic approach.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ameliorative effect of carvacrol on sodium arsenite-induced hepatotoxicity in rats: Possible role of Nrf2/HO-1, RAGE/NLRP3, Bax/Bcl-2/Caspase-3, and Beclin-1 pathways","authors":"Selman Gencer,&nbsp;Cihan Gür,&nbsp;Mustafa İleritürk,&nbsp;Sefa Küçükler,&nbsp;Nurhan Akaras,&nbsp;Hasan Şimşek,&nbsp;Fatih M. Kandemir","doi":"10.1002/jbt.23863","DOIUrl":"https://doi.org/10.1002/jbt.23863","url":null,"abstract":"<p>Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti-inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite-induced liver toxicity. Thirty-five <i>Sprague-Dawley</i> male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite-induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite-induced increased levels of NF-κB and the cytokines (TNF-α, IL-1β, IL-6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite-induced autophagic (Beclin-1, LC3A, and LC3B) and apoptotic (P53, Apaf-1, Casp-3, Casp-6, Casp-9, and Bax) parameters. Carvacrol preserved sodium arsenite-induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite-induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.23863","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sub-acute bisphenol A exposure induces proteomic alterations and impairs male reproductive health in mice","authors":"Shiv K. Yadav,&nbsp;Arvind Kumar,&nbsp;Bal G. Yadav,&nbsp;Vandana Bijalwan,&nbsp;Suresh Yadav,&nbsp;Gajanan P. Patil,&nbsp;Kamalesh Sarkar,&nbsp;Rajendra Palkhade,&nbsp;Santasabuj Das,&nbsp;Dhirendra P. Singh","doi":"10.1002/jbt.23862","DOIUrl":"https://doi.org/10.1002/jbt.23862","url":null,"abstract":"<p>Bisphenol A (BPA) is one of the most prevalent endocrine disrupting chemicals (EDCs) and there is widespread concern about the adverse effects of EDCs on human health. However, the exact mechanism of these toxicities has still not been fully deciphered. Additionally, studies have reported the toxicological effects at far low doses to the generally considered no-observed-adverse-effect level (NOAEL) dose. The present study investigates the effects of a sub-acute (28 days) exposure to BPA (10, 50 and 100 mg/kg/day) in adult male mice on various hormones levels, sperm motility, sperm count, functional integrity of sperm plasma membrane, testicular histological changes, oxidative stress markers and DNA damage. The key proteome signatures were quantified by LC-MS/MS analysis using Orbitrap Fusion Lumos Tribrid Mass Spectrometer equipped with nano-LC Easy-nLC 1200. Data suggest that the BPA exposure in all doses (below/above NOAEL dose) have greatly impacted the hormone levels, sperm parameters (sperm count, motility and membrane integrity) and testicular histology. Mass spectrometry-based proteomics data suggested for 1352 differentially expressed proteins (DEPs; 368 upregulated, 984 downregulated) affecting biological process, cellular component, and molecular functions. Specifically searched male reproductive function related proteins suggested a complex network where 46 potential proteins regulating spermatogenesis, sperm structure, activity and membrane integrity while tackling oxidative stress responses were downregulated. These potential biomarkers could shed some more light on our current understanding of the reproductive toxicological effects of BPA and may lead to exploration of novel interventions strategies against these targets for male infertility.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP1-mediated deubiquitination of KDM1A promotes the malignant progression of triple-negative breast cancer","authors":"Yang Su,&nbsp;Yan Du,&nbsp;Wenguang He","doi":"10.1002/jbt.23864","DOIUrl":"https://doi.org/10.1002/jbt.23864","url":null,"abstract":"<p>Previous research has indicated the highly expressed lysine-specific histone demethylase 1A (KDM1A) in several human malignancies, including triple-negative breast cancer (TNBC). However, its detailed mechanisms in TNBC development remain poorly understood. The mRNA levels of KDM1A and Yin Yang 1 (YY1) were determined by RT-qPCR analysis. Western blot was performed to measure KDM1A and ubiquitin-specific protease 1 (USP1) protein expression. Cell proliferation, apoptosis, invasion, migration and stemness were evaluated by MTT assay, EdU assay, flow cytometry, transwell invasion assay, wound-healing assay and sphere-formation assay, respectively. ChIP and dual-luciferase reporter assays were conducted to determine the relationship between YY1 and KDM1A. Xenograft tumor experiment and IHC were carried out to investigate the roles of USP1 and KDM1A in TNBC development in vivo. The highly expressed KDM1A was demonstrated in TNBC tissues and cells, and KDM1A knockdown significantly promoted cell apoptosis, and hampered cell proliferation, invasion, migration, and stemness in TNBC cells. USP1 could increase the stability of KDM1A via deubiquitination, and USP1 depletion restrained the progression of TNBC cells through decreasing KDM1A expression. Moreover, YY1 transcriptionally activated KDM1A expression by directly binding to its promoter in TNBC cells. Additionally, USP1 inhibition reduced KDM1A expression to suppress tumor growth in TNBC mice in vivo. In conclusion, YY1 upregulation increased KDM1A expression via transcriptional activation. USP1 stabilized KDM1A through deubiquitination to promote TNBC progression.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic anticancer effects and reduced genotoxicity of silver nanoparticles and tamoxifen in breast cancer cells","authors":"Maria D. Rivera,&nbsp;Rafael Vazquez-Duhalt,&nbsp;Ernestina Castro-Longoria,&nbsp;Karla Juarez-Moreno","doi":"10.1002/jbt.23823","DOIUrl":"10.1002/jbt.23823","url":null,"abstract":"<p>Nanotechnology is emerging as a promising tool to enhance traditional cancer treatments due to rising chemotherapy resistance and the severe side effects of toxic drugs. Silver nanoparticles (AgNPs) are widely acknowledged for their antimicrobial and antiproliferative properties. Given these AgNP characteristics, this research conducts a comprehensive nanotoxicological assessment of strategic combinations involving AgNPs (68 nm) commercial formulation and tamoxifen on MCF-7 and MDA-MB-231 breast tumor cells. Utilizing CompuSyn software, the combination index was determined, revealing a synergistic cytotoxic and antiproliferative effect in AgNPs and tamoxifen combinations (CI &lt; 0.97). Furthermore, this combination impaired cell migration (the scratch zone expanded by over 270%) and significantly increased reactive oxygen species production (up to 96% for MDA-MB-231 and 52% for MCF-7 cells). Surprisingly, the genotoxic effect of these mixtures was minimal (below the allowable genotoxicity index of 1.5). Additionally, both breast tumor cell lines exhibited increased proapoptotic and oxidative stress gene expression following the combined treatment. The internalization of AgNPs into breast cancer cells was observed, enhancing their synergistic antiproliferative effect when combined with tamoxifen. These findings suggest the potential of combining AgNPs with chemotherapeutic agents for innovative studies in oncology therapy.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.23823","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cynaropicrin attenuates inflammatory cytokines in LPS-induced RAW264.7 cells and ovalbumin-induced asthmatic mice","authors":"Junyan Chen,&nbsp;Xiaohong Liu","doi":"10.1002/jbt.23836","DOIUrl":"10.1002/jbt.23836","url":null,"abstract":"<p>This study examines the anti-inflammatory activity of cynaropicrin against lipopolysaccharide (LPS) in vitro and ovalbumin (OVA)-challenged asthma in mice. Cynaropicrin's antimicrobial effects were tested on <i>Escherichia coli (E. coli)</i> and <i>Streptococcus pyogenes (S. pyogenes)</i> using the disc diffusion technique. Cytotoxicity was assessed with an (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay. The anti-inflammatory property was evaluated in LPS-induced RAW264.7 cells, while OVA-challenged asthmatic mice were treated with 10 mg/kg of cynaropicrin. Key inflammatory and antioxidant markers were quantified, and lung histology was examined to confirm therapeutic roles. The antimicrobial studies proved that cynaropicrin effectively inhibited the growth of <i>E. coli</i> and <i>S. pyogenes</i>. Cynaropicrin displayed no cytotoxicity on RAW264.7 cells. Furthermore, it significantly inhibited inflammatory cytokine synthesis upon LPS induction. Cynaropicrin treatment decreased the inflammatory cell counts and also suppressed specific allergic markers in OVA-challenged mice. It also decreased nitric oxide and myeloperoxidase levels and reduced pulmonary edema. Cynaropicrin increased antioxidant levels and decreased proinflammatory cytokines in the asthmatic mice. Lung histological examination confirms the ameliorative potency of cynaropicrin against OVA-induced asthmatic pulmonary inflammation in mice. Our findings suggest cynaropicrin possesses significant ameliorative potency against allergen-induced pulmonary inflammation.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}