首页 > 最新文献

Environmental Toxicology最新文献

英文 中文
RETRACTION: USP14 Promotes the Proliferation of Cervical Cancer via Upregulating β‐Catenin
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24493
RETRACTION: H. Song, J. Qiu, and K. Hua, “USP14 Promotes the Proliferation of Cervical Cancer via Upregulating β‐Catenin,” Environmental Toxicology 39, no. 2 (2024): 1031‐1043, https://doi.org/10.1002/tox.23990.The above article, published online on 9 December 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.
{"title":"RETRACTION: USP14 Promotes the Proliferation of Cervical Cancer via Upregulating β‐Catenin","authors":"","doi":"10.1002/tox.24493","DOIUrl":"https://doi.org/10.1002/tox.24493","url":null,"abstract":"RETRACTION: H. Song, J. Qiu, and K. Hua, “USP14 Promotes the Proliferation of Cervical Cancer via Upregulating β‐Catenin,” <jats:italic>Environmental Toxicology</jats:italic> 39, no. 2 (2024): 1031‐1043, <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.23990\">https://doi.org/10.1002/tox.23990</jats:ext-link>.The above article, published online on 9 December 2023, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"6 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427171","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}
引用次数: 0
RETRACTION: Zinc Finger Protein207 Orchestrates Glioma Migration Through Regulation of Epithelial‐Mesenchymal Transition
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24496
RETRACTION: C. Zhao, Y. Guo, Y. Chen, G. Shang, D. Song, J. Wang, J. Yang, and H. Zhang, “Zinc Finger Protein207 Orchestrates Glioma Migration Through Regulation of Epithelial‐Mesenchymal Transition,” Environmental Toxicology (EarlyView): https://doi.org/10.1002/tox.24271.The above article, published online on 9 April 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.
{"title":"RETRACTION: Zinc Finger Protein207 Orchestrates Glioma Migration Through Regulation of Epithelial‐Mesenchymal Transition","authors":"","doi":"10.1002/tox.24496","DOIUrl":"https://doi.org/10.1002/tox.24496","url":null,"abstract":"RETRACTION: C. Zhao, Y. Guo, Y. Chen, G. Shang, D. Song, J. Wang, J. Yang, and H. Zhang, “Zinc Finger Protein207 Orchestrates Glioma Migration Through Regulation of Epithelial‐Mesenchymal Transition,” <jats:italic>Environmental Toxicology</jats:italic> (EarlyView): <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24271\">https://doi.org/10.1002/tox.24271</jats:ext-link>.The above article, published online on 9 April 2024, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"51 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143435154","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}
引用次数: 0
RETRACTION: MiR‐375 Impairs Breast Cancer Cell Stemness by Targeting the KLF5/G6PD Signaling Axis
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24494
RETRACTON: H. Chen, S. Hou, H. Zhang, B. Zhou, H. Xi, X. Li, Z. Lufeng, and Q. Guo, “MiR‐375 Impairs Breast Cancer Cell Stemness by Targeting the KLF5/G6PD Signaling Axis,” Environmental Toxicology (EarlyView): https://doi.org/10.1002/tox.24204.The above article, published online on 12 March 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The authors Haitao Chen, Qianqian Guo, and Lufeng Zheng disagree with this decision. Qianqian Guo, Haitao Chen, and Zheng Lufeng disagree with this decision.
{"title":"RETRACTION: MiR‐375 Impairs Breast Cancer Cell Stemness by Targeting the KLF5/G6PD Signaling Axis","authors":"","doi":"10.1002/tox.24494","DOIUrl":"https://doi.org/10.1002/tox.24494","url":null,"abstract":"RETRACTON: H. Chen, S. Hou, H. Zhang, B. Zhou, H. Xi, X. Li, Z. Lufeng, and Q. Guo, “MiR‐375 Impairs Breast Cancer Cell Stemness by Targeting the KLF5/G6PD Signaling Axis,” <jats:italic>Environmental Toxicology</jats:italic> (EarlyView): <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24204\">https://doi.org/10.1002/tox.24204</jats:ext-link>.The above article, published online on 12 March 2024, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The authors Haitao Chen, Qianqian Guo, and Lufeng Zheng disagree with this decision. Qianqian Guo, Haitao Chen, and Zheng Lufeng disagree with this decision.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"24 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143435207","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}
引用次数: 0
RETRACTION: Development of Gene Panel for Predicting Recurrence in Early‐Stage Cervical Cancer Patients
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24495
RETRACTION: Y. Ma and W. Zhu, “Development of Gene Panel for Predicting Recurrence in Early‐Stage Cervical Cancer Patients,” Environmental Toxicology (EarlyView): https://doi.org/10.1002/tox.24270.The above article, published online on 2 April 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. Weipei Zhu disagrees with this decision.
{"title":"RETRACTION: Development of Gene Panel for Predicting Recurrence in Early‐Stage Cervical Cancer Patients","authors":"","doi":"10.1002/tox.24495","DOIUrl":"https://doi.org/10.1002/tox.24495","url":null,"abstract":"RETRACTION: Y. Ma and W. Zhu, “Development of Gene Panel for Predicting Recurrence in Early‐Stage Cervical Cancer Patients,” <jats:italic>Environmental Toxicology</jats:italic> (EarlyView): <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24270\">https://doi.org/10.1002/tox.24270</jats:ext-link>.The above article, published online on 2 April 2024, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. Weipei Zhu disagrees with this decision.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"80 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143435210","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}
引用次数: 0
RETRACTION: Leptin Receptor Gln223Arg and Lys109Arg Polymorphisms May Be Associated With HBV‐Related Hepatocellular Carcinoma Risk: A System Review and Meta‐Analysis 检索:瘦素受体 Gln223Arg 和 Lys109Arg 多态性可能与 HBV 相关肝细胞癌风险有关:系统综述与元分析
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24497
RETRACTION: X. Dong, M. Zou, C. Li, H. Luo, S. Zhu, and Z. Gong, “Leptin Receptor Gln223Arg and Lys109Arg Polymorphisms May Be Associated with HBV‐Related Hepatocellular Carcinoma Risk: A System Review and Meta‐Analysis,” Environmental Toxicology 39, no. 10 (2024): 4623‐4634, https://doi.org/10.1002/tox.24286.The above article, published online on 18 April 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The author Shaoliang Zhu disagrees with this decision.
{"title":"RETRACTION: Leptin Receptor Gln223Arg and Lys109Arg Polymorphisms May Be Associated With HBV‐Related Hepatocellular Carcinoma Risk: A System Review and Meta‐Analysis","authors":"","doi":"10.1002/tox.24497","DOIUrl":"https://doi.org/10.1002/tox.24497","url":null,"abstract":"RETRACTION: X. Dong, M. Zou, C. Li, H. Luo, S. Zhu, and Z. Gong, “Leptin Receptor <jats:italic>Gln223Arg</jats:italic> and <jats:italic>Lys109Arg</jats:italic> Polymorphisms May Be Associated with HBV‐Related Hepatocellular Carcinoma Risk: A System Review and Meta‐Analysis,” <jats:italic>Environmental Toxicology</jats:italic> 39, no. 10 (2024): 4623‐4634, <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"https://doi.org/10.1002/tox.24286\">https://doi.org/10.1002/tox.24286</jats:ext-link>.The above article, published online on 18 April 2024, in Wiley Online Library (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://onlinelibrary.wiley.com/\">http://onlinelibrary.wiley.com/</jats:ext-link>), has been retracted by agreement between the journal Editor‐in‐Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The author Shaoliang Zhu disagrees with this decision.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"46 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427032","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}
引用次数: 0
Effects of D‐Tetramethrin on Zebrafish Development and Immune System
IF 4.5 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-17 DOI: 10.1002/tox.24487
Yang Li, Keyuan Zhong, Sijie Zhang, Shiyi Duan, Kaijie Huang, Xiaofang Che, Xinchun Guo, Huiqiang Lu
D‐tetramethrin is a common insecticide that is important for the control of mosquito‐transmitted diseases such as malaria and dengue and, due to its widespread use, it is frequently detected in environmental systems. However, there is currently very little information on the influence of D‐tetramethrin on non‐target organisms. In this study, zebrafish embryos were exposed to various concentrations of D‐tetramethrin (0, 3, 6, and 9 mg/L) from 6 to 72 h past fertilization (hpf) to ascertain the influence of D‐tetramethrin on the zebrafish immune system and development. We found that D‐tetramethrin exposure led to a significant decrease in heart rate, an increase in the yolk area and tail flick frequency, and a shortening of body length in zebrafish larvae, compared with the control group. The number of macrophages and neutrophils in the experimental group of zebrafish larvae decreased significantly and the oxidative stress levels increased compared with the control group. The malondialdehyde (MDA) content and reactive oxygen species (ROS) content increased significantly, while catalase (CAT) activity increased and superoxide dismutase (SOD) activity decreased in the experimental group. At the same time, apoptosis increased in the zebrafish embryo cells, and the expression of apoptosis‐related genes such as p53, Bax, and Bcl‐2 was abnormal. Moreover, the pro‐inflammatory genes IL‐8, IFN‐γ, IL‐6, and TNF‐α were up‐regulated, while the anti‐inflammatory gene, IL‐10, was down‐regulated. Therefore, D‐tetramethrin significantly affects the immune system and oxidative stress levels in zebrafish, inducing cell apoptosis and negatively affecting embryo development. These results provide novel data for the toxicity of D‐tetramethrin and the potential adverse effects of environment residues.
{"title":"Effects of D‐Tetramethrin on Zebrafish Development and Immune System","authors":"Yang Li, Keyuan Zhong, Sijie Zhang, Shiyi Duan, Kaijie Huang, Xiaofang Che, Xinchun Guo, Huiqiang Lu","doi":"10.1002/tox.24487","DOIUrl":"https://doi.org/10.1002/tox.24487","url":null,"abstract":"D‐tetramethrin is a common insecticide that is important for the control of mosquito‐transmitted diseases such as malaria and dengue and, due to its widespread use, it is frequently detected in environmental systems. However, there is currently very little information on the influence of D‐tetramethrin on non‐target organisms. In this study, zebrafish embryos were exposed to various concentrations of D‐tetramethrin (0, 3, 6, and 9 mg/L) from 6 to 72 h past fertilization (hpf) to ascertain the influence of D‐tetramethrin on the zebrafish immune system and development. We found that D‐tetramethrin exposure led to a significant decrease in heart rate, an increase in the yolk area and tail flick frequency, and a shortening of body length in zebrafish larvae, compared with the control group. The number of macrophages and neutrophils in the experimental group of zebrafish larvae decreased significantly and the oxidative stress levels increased compared with the control group. The malondialdehyde (MDA) content and reactive oxygen species (ROS) content increased significantly, while catalase (CAT) activity increased and superoxide dismutase (SOD) activity decreased in the experimental group. At the same time, apoptosis increased in the zebrafish embryo cells, and the expression of apoptosis‐related genes such as <jats:italic>p53</jats:italic>, <jats:italic>Bax</jats:italic>, and <jats:italic>Bcl‐2</jats:italic> was abnormal. Moreover, the pro‐inflammatory genes <jats:italic>IL‐8</jats:italic>, <jats:italic>IFN‐γ</jats:italic>, <jats:italic>IL‐6</jats:italic>, and <jats:italic>TNF‐α</jats:italic> were up‐regulated, while the anti‐inflammatory gene, <jats:italic>IL‐10</jats:italic>, was down‐regulated. Therefore, D‐tetramethrin significantly affects the immune system and oxidative stress levels in zebrafish, inducing cell apoptosis and negatively affecting embryo development. These results provide novel data for the toxicity of D‐tetramethrin and the potential adverse effects of environment residues.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"11 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143435155","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}
引用次数: 0
RETRACTION: NIK-Mediated Reactivation of SIX2 Enhanced the CSC-like Traits of Hepatocellular Carcinoma Cells Through Suppressing Ubiquitin–Proteasome System 回归:NIK 介导的 SIX2 重激活通过抑制泛素-蛋白酶体系统增强了肝细胞癌细胞的 CSC 样性状
IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-16 DOI: 10.1002/tox.24492

RETRACTION: L. Daren, Y. Dan, W. Jinhong, and L. Chao, “NIK-Mediated Reactivation of SIX2 Enhanced the CSC-like Traits of Hepatocellular Carcinoma Cells Through Suppressing Ubiquitin–Proteasome System,” Environmental Toxicology 39, no. 2 (2024): 583-591, https://doi.org/10.1002/tox.23892.

The above article, published online on 17 July 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.

{"title":"RETRACTION: NIK-Mediated Reactivation of SIX2 Enhanced the CSC-like Traits of Hepatocellular Carcinoma Cells Through Suppressing Ubiquitin–Proteasome System","authors":"","doi":"10.1002/tox.24492","DOIUrl":"10.1002/tox.24492","url":null,"abstract":"<p>\u0000 <b>RETRACTION:</b> L. Daren, Y. Dan, W. Jinhong, and L. Chao, “NIK-Mediated Reactivation of SIX2 Enhanced the CSC-like Traits of Hepatocellular Carcinoma Cells Through Suppressing Ubiquitin–Proteasome System,” <i>Environmental Toxicology</i> 39, no. 2 (2024): 583-591, https://doi.org/10.1002/tox.23892.</p><p>The above article, published online on 17 July 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 4","pages":"717"},"PeriodicalIF":4.4,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143427031","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}
引用次数: 0
Methylmercury Chronic Exposure and a High-Fat Diet Induce Gut Microbiome Alterations and Intestinal Barrier Disruption in Mice.
IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-02-08 DOI: 10.1002/tox.24469
Gabriella A Matos, Daniela Nunes-Costa, Daniel V Pinto, Conceição S Martins, Janayne L Silva, Paola Caroline Lacerda Leocadio, Maria Emília Rabelo Andrade, Ramon S Raposo, Igor Tiago, Susana Alarico, Elandia A Santos, Valbert Nascimento Cardoso, Flávia A Santos, Jacqueline I Alvarez-Leite, Nuno Empadinhas, Reinaldo B Oriá

Methylmercury (MeHg) is markedly toxic to humans. Our study explores whether MeHg and high-fat diet (HFD) can impair the intestinal barrier with microbiota dysbiosis in mice. Weanling mice were fed to HFD or standard diet for 40 days. In the last 20 days of diets, mice received either MeHg (20 mg/L) or drinking water. Proximal small intestine, cecum, and hair samples were collected. Villus length, crypt depth, villus/crypt length, mucin2 and lysozyme-positive cell counts, ZO-1 and occludin gene expression, and intestinal functional permeability were analyzed to assess the intestinal barrier. Blood samples were drawn to assess lipid parameters. Gut microbiome profiling was conducted with DNA from fecal/cecal samples. In addition, we analyzed ZO-1 immunofluorescence in the colon and small intestine. HFD increased MDA, Mucin2, and reduced villus height, crypt depth, villus/crypt length, lysozyme(+)-cell count, and increased intestinal permeability, regardless of MeHg intoxication. MeHg-HFD combination affected the intestinal barrier, decreasing ZO-1, occludin, and Nrf2 transcription, and increased permeability. HFD increased total plasma cholesterol and triglycerides. Only MeHg-HFD reduced microbiome alpha-diversity along with colonic ZO-1 immunolabeling loss compared to non-intoxicated mice fed a control diet. Regardless of diet, the genera Streptococcus, Psychrobacter, Facklamia, and Corynebacterium were severely depleted following MeHg intoxication. Other groups, such as Atopostipes and Jeotgalicoccus, were not altered by MeHg or HFD alone, but were significantly reduced by the combined HFD-MeHg. Synergistic effects of MeHg-HFD on the mucosa-associated microbiota are more pronounced than their individual effects. Our findings suggest that MeHg intoxication does not cause extensive dysbiosis but led to intestinal barrier disruption.

{"title":"Methylmercury Chronic Exposure and a High-Fat Diet Induce Gut Microbiome Alterations and Intestinal Barrier Disruption in Mice.","authors":"Gabriella A Matos, Daniela Nunes-Costa, Daniel V Pinto, Conceição S Martins, Janayne L Silva, Paola Caroline Lacerda Leocadio, Maria Emília Rabelo Andrade, Ramon S Raposo, Igor Tiago, Susana Alarico, Elandia A Santos, Valbert Nascimento Cardoso, Flávia A Santos, Jacqueline I Alvarez-Leite, Nuno Empadinhas, Reinaldo B Oriá","doi":"10.1002/tox.24469","DOIUrl":"https://doi.org/10.1002/tox.24469","url":null,"abstract":"<p><p>Methylmercury (MeHg) is markedly toxic to humans. Our study explores whether MeHg and high-fat diet (HFD) can impair the intestinal barrier with microbiota dysbiosis in mice. Weanling mice were fed to HFD or standard diet for 40 days. In the last 20 days of diets, mice received either MeHg (20 mg/L) or drinking water. Proximal small intestine, cecum, and hair samples were collected. Villus length, crypt depth, villus/crypt length, mucin2 and lysozyme-positive cell counts, ZO-1 and occludin gene expression, and intestinal functional permeability were analyzed to assess the intestinal barrier. Blood samples were drawn to assess lipid parameters. Gut microbiome profiling was conducted with DNA from fecal/cecal samples. In addition, we analyzed ZO-1 immunofluorescence in the colon and small intestine. HFD increased MDA, Mucin2, and reduced villus height, crypt depth, villus/crypt length, lysozyme(+)-cell count, and increased intestinal permeability, regardless of MeHg intoxication. MeHg-HFD combination affected the intestinal barrier, decreasing ZO-1, occludin, and Nrf2 transcription, and increased permeability. HFD increased total plasma cholesterol and triglycerides. Only MeHg-HFD reduced microbiome alpha-diversity along with colonic ZO-1 immunolabeling loss compared to non-intoxicated mice fed a control diet. Regardless of diet, the genera Streptococcus, Psychrobacter, Facklamia, and Corynebacterium were severely depleted following MeHg intoxication. Other groups, such as Atopostipes and Jeotgalicoccus, were not altered by MeHg or HFD alone, but were significantly reduced by the combined HFD-MeHg. Synergistic effects of MeHg-HFD on the mucosa-associated microbiota are more pronounced than their individual effects. Our findings suggest that MeHg intoxication does not cause extensive dysbiosis but led to intestinal barrier disruption.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373923","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}
引用次数: 0
Revolutionizing prognosis: Introducing cell death index (CDI) as a powerful prognostic tool for CSCC patients
IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-01-31 DOI: 10.1002/tox.24265
Rongjun Tang, Qing Yao, Ke Zhang, Qingqing Yu, Jun Lou, Lingdi Li

Background

Cervical squamous cell carcinoma (CSCC) threatens the body health of women worldwide. This study aimed to foster a new concept of prognostic indicator named cell death index (CDI).

Methods

RNA-seq and scRNA-seq datasets were downloaded from the GEO and TCGA database as the training and validation cohorts. Programmed cell death (PCD)-related gene signatures were obtained from published research. The construction of prognostic model was performed based on CDI value. Patients with CSCC were divided into high- and low-CDI groups. We explored the differences in overall survival time, immune infiltration, mutation status, and drug sensitivity between high and low CDI groups by R software.

Results

We constructed prognostic model to calculate the CDI value with 23 genes. Patients with high CDI have shorter survival time than those with low CDI. CDI was considered a risk factor compared to other characteristics. The nomogram model estimated overall survival (OS) at 1, 3, and 6 years, with age, Stage, and CDI, indicating the accuracy of the model in predicting 1-, 3-, and 6-year survival rates. CDI values were negatively correlated with most immune checkpoint genes. We measured the significant drug sensitivity of Mitoxantrone, Sabutoclax, Sepantronium bromide, Topotecan, BI-2536, and BMS-754807 between high- and low-CDI groups with significant correlation.

Conclusion

This investigation constructed a novel effective prognostic indicator of CDI in patients with CSCC and identified potential genes associated with cell death that could be targeted for prognosis and treatment of CSCC.

{"title":"Revolutionizing prognosis: Introducing cell death index (CDI) as a powerful prognostic tool for CSCC patients","authors":"Rongjun Tang,&nbsp;Qing Yao,&nbsp;Ke Zhang,&nbsp;Qingqing Yu,&nbsp;Jun Lou,&nbsp;Lingdi Li","doi":"10.1002/tox.24265","DOIUrl":"10.1002/tox.24265","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cervical squamous cell carcinoma (CSCC) threatens the body health of women worldwide. This study aimed to foster a new concept of prognostic indicator named cell death index (CDI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>RNA-seq and scRNA-seq datasets were downloaded from the GEO and TCGA database as the training and validation cohorts. Programmed cell death (PCD)-related gene signatures were obtained from published research. The construction of prognostic model was performed based on CDI value. Patients with CSCC were divided into high- and low-CDI groups. We explored the differences in overall survival time, immune infiltration, mutation status, and drug sensitivity between high and low CDI groups by R software.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We constructed prognostic model to calculate the CDI value with 23 genes. Patients with high CDI have shorter survival time than those with low CDI. CDI was considered a risk factor compared to other characteristics. The nomogram model estimated overall survival (OS) at 1, 3, and 6 years, with age, Stage, and CDI, indicating the accuracy of the model in predicting 1-, 3-, and 6-year survival rates. CDI values were negatively correlated with most immune checkpoint genes. We measured the significant drug sensitivity of Mitoxantrone, Sabutoclax, Sepantronium bromide, Topotecan, BI-2536, and BMS-754807 between high- and low-CDI groups with significant correlation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This investigation constructed a novel effective prognostic indicator of CDI in patients with CSCC and identified potential genes associated with cell death that could be targeted for prognosis and treatment of CSCC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 3","pages":"481-492"},"PeriodicalIF":4.4,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064578","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}
引用次数: 0
The role and mechanism of hepatocyte nuclear factor 1β in the occurrence and development of different human tumors: A pan-cancer analysis
IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES Pub Date : 2025-01-31 DOI: 10.1002/tox.24254
Liang Li, Haikun Li, Ke Zhang, Chunchun Zhao, Fei Wang, Jian Sun, Jianqing Wang

Carcinomatosis is one of the leading threats to human public fitness. HNF1B is a critical transcription element in vertebrate proliferation and oncogenesis, which has been shown to play roles in reactive oxygen species (ROS) metabolism. Our previous results have identified HNF1B as a tumor suppressor that could inhibit the malignant progression of prostate cancer. Yet there is no pan-carcinomatosis analysis of HNF1B, which could help us better understand common and unique underlying mechanisms in mankind knubs to enhance novel and competent treatment. Here, in our research, we evaluated the utterance pattern and explored the function of HNF1B in 33 knub categories using the data from the Cancer Genome Atlas Program (TCGA), Gene Expression Omnibus (GEO), and CLNICAL PROTEOMICTUMOR ANALYSIS CONSORTIUM (CPTAC) dataset. We found different HNF1B roles in various cancer types. HNF1B was upregulated in CHOL, STAD, KIRP, and THCA, and was downregulated in GBM, KICH, COAD, KIRC, LUSC, SARC, PAAD, and TGCT. Prognostic analyses indicated that higher HNF1B displayed better illness outcomes in BLCA, READ, and PRAD, while poorer outcomes in LUSC and THYM. HNF1B mutation was most frequent in endometrial cancer but was not associated with disease prognosis. It was discovered that HNF1B utterance relevant to endothelial cell penetration status in BLCA, ESCA, LUAD, LUSC, and TGCT, and carcinomatosis-associated fibroblast infiltration was observed in ESCA, KIRC, LIHC, and TGCT. Moreover, functional enrichment analysis disclosed that metabolism-related functions were implicated in the function of HNF1B. Taken together, our pan- carcinomatosis analysis showed the complicated roles of HNF1B in a variety of carcinomatoses, being able to improve the extensive comprehension of HNF1B's role in tumorigenesis.

{"title":"The role and mechanism of hepatocyte nuclear factor 1β in the occurrence and development of different human tumors: A pan-cancer analysis","authors":"Liang Li,&nbsp;Haikun Li,&nbsp;Ke Zhang,&nbsp;Chunchun Zhao,&nbsp;Fei Wang,&nbsp;Jian Sun,&nbsp;Jianqing Wang","doi":"10.1002/tox.24254","DOIUrl":"10.1002/tox.24254","url":null,"abstract":"<p>Carcinomatosis is one of the leading threats to human public fitness. HNF1B is a critical transcription element in vertebrate proliferation and oncogenesis, which has been shown to play roles in reactive oxygen species (ROS) metabolism. Our previous results have identified HNF1B as a tumor suppressor that could inhibit the malignant progression of prostate cancer. Yet there is no pan-carcinomatosis analysis of HNF1B, which could help us better understand common and unique underlying mechanisms in mankind knubs to enhance novel and competent treatment. Here, in our research, we evaluated the utterance pattern and explored the function of HNF1B in 33 knub categories using the data from the Cancer Genome Atlas Program (TCGA), Gene Expression Omnibus (GEO), and CLNICAL PROTEOMICTUMOR ANALYSIS CONSORTIUM (CPTAC) dataset. We found different HNF1B roles in various cancer types. HNF1B was upregulated in CHOL, STAD, KIRP, and THCA, and was downregulated in GBM, KICH, COAD, KIRC, LUSC, SARC, PAAD, and TGCT. Prognostic analyses indicated that higher HNF1B displayed better illness outcomes in BLCA, READ, and PRAD, while poorer outcomes in LUSC and THYM. HNF1B mutation was most frequent in endometrial cancer but was not associated with disease prognosis. It was discovered that HNF1B utterance relevant to endothelial cell penetration status in BLCA, ESCA, LUAD, LUSC, and TGCT, and carcinomatosis-associated fibroblast infiltration was observed in ESCA, KIRC, LIHC, and TGCT. Moreover, functional enrichment analysis disclosed that metabolism-related functions were implicated in the function of HNF1B. Taken together, our pan- carcinomatosis analysis showed the complicated roles of HNF1B in a variety of carcinomatoses, being able to improve the extensive comprehension of HNF1B's role in tumorigenesis.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 3","pages":"471-480"},"PeriodicalIF":4.4,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064584","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}
引用次数: 0
期刊
Environmental Toxicology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1