RETRACTION: J. Chen, “ Regulatory Mechanism of RNA Binding Motif Protein 15-Mediated N6 Methyladenosine Modification in Proliferation, Invasion, and Migration of Colorectal Cancer Cells,” Environmental Toxicology38, no. 11 (2023): 2545–2559, https://doi.org/10.1002/tox.23883.
The above article, published online on 20 July 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; and Wiley Periodicals LLC.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.
Author J. Chen did not respond to communications from the Publisher regarding the retraction.
{"title":"RETRACTION: Regulatory Mechanism of RNA Binding Motif Protein 15-Mediated N6 Methyladenosine Modification in Proliferation, Invasion, and Migration of Colorectal Cancer Cells","authors":"","doi":"10.1002/tox.24598","DOIUrl":"10.1002/tox.24598","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>J. Chen</span>, “ <span>Regulatory Mechanism of RNA Binding Motif Protein 15-Mediated N<sup>6</sup> Methyladenosine Modification in Proliferation, Invasion, and Migration of Colorectal Cancer Cells</span>,” <i>Environmental Toxicology</i> <span>38</span>\u0000 <i>,</i> no. <span>11</span> (<span>2023</span>): <span>2545</span>–<span>2559</span>, https://doi.org/10.1002/tox.23883.\u0000 </p><p>The above article, published online on 20 July 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; and Wiley Periodicals LLC.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><p>Author J. Chen did not respond to communications from the Publisher regarding the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24598","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145354154","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}
RETRACTION: C. Hacioglu, F. Kar, F. Davran, and C. Tuncer, “ Borax Regulates Iron Chaperone- and Autophagy-Mediated Ferroptosis Pathway in Glioblastoma Cells,” Environmental Toxicology38, no. 7 (2023): 1690–1701, https://doi.org/10.1002/tox.23797.
The above article, published online on 29 March 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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 disagree with the retraction.
C. Hacioglu， F. Kar， F. Davran， C. Tuncer，“硼砂调节铁伴侣蛋白和自噬介导的胶质母细胞瘤细胞铁凋亡途径，”环境毒理学38，no。7 (2023): 1690-1701, https://doi.org/10.1002/tox.23797。上述文章于2023年3月29日在线发表在Wiley在线图书馆（http://onlinelibrary.wiley.com/）上，经期刊主编April Rodd；和Wiley期刊有限责任公司。经过出版商的调查，双方得出结论，这篇文章完全是在妥协的同行评议过程的基础上被接受的。因此，这篇文章必须撤回。作者不同意撤稿。
{"title":"RETRACTION: Borax Regulates Iron Chaperone- and Autophagy-Mediated Ferroptosis Pathway in Glioblastoma Cells","authors":"","doi":"10.1002/tox.24594","DOIUrl":"10.1002/tox.24594","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>C. Hacioglu</span>, <span>F. Kar</span>, <span>F. Davran</span>, and <span>C. Tuncer</span>, “ <span>Borax Regulates Iron Chaperone- and Autophagy-Mediated Ferroptosis Pathway in Glioblastoma Cells</span>,” <i>Environmental Toxicology</i> <span>38</span>, no. <span>7</span> (<span>2023</span>): <span>1690</span>–<span>1701</span>, https://doi.org/10.1002/tox.23797.\u0000 </p><p>The above article, published online on 29 March 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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><p>The authors disagree with the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351860","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}
RETRACTION: V. Karuppaiya, A. Annamalai, S. Krishnamurthy, and K. Soundarapandian, “ Dieckol Prevents Prostate Cancer Cell Proliferation by Transcriptionally Attenuating JAK/STAT3 Signaling Pathway,” Environmental Toxicology39, no. 3 (2024): 1187–1196, https://doi.org/10.1002/tox.24006.
The above article, published online on 27 October 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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.
Author V. Karuppaiya agrees with the retraction. Authors A. Annamalai and K. Soundarapandian did not respond to communications from the Publisher regarding the retraction. Author S. Krishnamurthy could not be reached for comment regarding the retraction.
引用本文：V. Karuppaiya， A. Annamalai， S. Krishnamurthy， K. Soundarapandian，“通过转录抑制JAK/STAT3信号通路，Dieckol抑制前列腺癌细胞增殖”，环境毒理学，39,no。3 (2024): 1187-1196, https://doi.org/10.1002/tox.24006。上述文章于2023年10月27日在线发表在Wiley在线图书馆（http://onlinelibrary.wiley.com/）上，经期刊主编April Rodd；和Wiley期刊有限责任公司。经过出版商的调查，双方得出结论，这篇文章完全是在妥协的同行评议过程的基础上被接受的。因此，这篇文章必须撤回。作者V. Karuppaiya同意撤稿。作者A. Annamalai和K. Soundarapandian没有回应出版商关于撤稿的联系。记者无法联系到作者S. Krishnamurthy就撤稿一事发表评论。
{"title":"RETRACTION: Dieckol Prevents Prostate Cancer Cell Proliferation by Transcriptionally Attenuating JAK/STAT3 Signaling Pathway","authors":"","doi":"10.1002/tox.24585","DOIUrl":"10.1002/tox.24585","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>V. Karuppaiya</span>, <span>A. Annamalai</span>, <span>S. Krishnamurthy</span>, and <span>K. Soundarapandian</span>, “ <span>Dieckol Prevents Prostate Cancer Cell Proliferation by Transcriptionally Attenuating JAK/STAT3 Signaling Pathway</span>,” <i>Environmental Toxicology</i> <span>39</span>, no. <span>3</span> (<span>2024</span>): <span>1187</span>–<span>1196</span>, https://doi.org/10.1002/tox.24006.\u0000 </p><p>The above article, published online on 27 October 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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><p>Author V. Karuppaiya agrees with the retraction. Authors A. Annamalai and K. Soundarapandian did not respond to communications from the Publisher regarding the retraction. Author S. Krishnamurthy could not be reached for comment regarding the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24585","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145354057","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}
RETRACTION: H. Gong, L. Zhao, and J. Liu, “ Protective Effect of Tretinoin on Cervical Cancer Growth and Proliferation Through Downregulation of pFAK2 Expression,” Environmental Toxicology39, no. 5 (2024): 2732–2740, https://doi.org/10.1002/tox.24144.
The above article, published online on 22 January 2024 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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.
Author J. Liu did not respond to communications from the Publisher regarding the retraction. Authors H. Gong and L. Zhao could not be reached for comment regarding the retraction.
{"title":"RETRACTION: Protective Effect of Tretinoin on Cervical Cancer Growth and Proliferation Through Downregulation of pFAK2 Expression","authors":"","doi":"10.1002/tox.24587","DOIUrl":"10.1002/tox.24587","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>H. Gong</span>, <span>L. Zhao</span>, and <span>J. Liu</span>, “ <span>Protective Effect of Tretinoin on Cervical Cancer Growth and Proliferation Through Downregulation of pFAK2 Expression</span>,” <i>Environmental Toxicology</i> <span>39</span>, no. <span>5</span> (<span>2024</span>): <span>2732</span>–<span>2740</span>, https://doi.org/10.1002/tox.24144.\u0000 </p><p>The above article, published online on 22 January 2024 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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><p>Author J. Liu did not respond to communications from the Publisher regarding the retraction. Authors H. Gong and L. Zhao could not be reached for comment regarding the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24587","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145354152","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}
RETRACTION: Y. Tian, W. Han, L. Fu, K. Lv, and X. Zhou, “ Silencing of IGHG1 Reverses the Resistance of Pancreatic Cancer to Multidrug Chemotherapy by Modulating Autophagy,” Environmental Toxicology38, no. 8 (2023): 1835–1845, https://doi.org/10.1002/tox.23810.
The above article, published online on 26 April 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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 did not respond to communications from the Publisher regarding the retraction.
{"title":"RETRACTION: Silencing of IGHG1 Reverses the Resistance of Pancreatic Cancer to Multidrug Chemotherapy by Modulating Autophagy","authors":"","doi":"10.1002/tox.24596","DOIUrl":"10.1002/tox.24596","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>Y. Tian</span>, <span>W. Han</span>, <span>L. Fu</span>, <span>K. Lv</span>, and <span>X. Zhou</span>, “ <span>Silencing of IGHG1 Reverses the Resistance of Pancreatic Cancer to Multidrug Chemotherapy by Modulating Autophagy</span>,” <i>Environmental Toxicology</i> <span>38</span>, no. <span>8</span> (<span>2023</span>): <span>1835</span>–<span>1845</span>, https://doi.org/10.1002/tox.23810.\u0000 </p><p>The above article, published online on 26 April 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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><p>The authors did not respond to communications from the Publisher regarding the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24596","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145354155","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}
RETRACTION: Y. Lin, P. Lin, W. Guo, J. Huang, X. Xu, and X. Zhuang, “ PLAGL2 Promotes the Stemness and is Upregulated by Transcription Factor E2F1 in Human Lung Cancer,” Environmental Toxicology38, no. 4 (2023): 941–949, https://doi.org/10.1002/tox.23739.
The above article, published online on 09 January 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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 did not respond to communications from the Publisher regarding the retraction.
{"title":"RETRACTION: PLAGL2 Promotes the Stemness and is Upregulated by Transcription Factor E2F1 in Human Lung Cancer","authors":"","doi":"10.1002/tox.24591","DOIUrl":"10.1002/tox.24591","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>Y. Lin</span>, <span>P. Lin</span>, <span>W. Guo</span>, <span>J. Huang</span>, <span>X. Xu</span>, and <span>X. Zhuang</span>, “ <span>PLAGL2 Promotes the Stemness and is Upregulated by Transcription Factor E2F1 in Human Lung Cancer</span>,” <i>Environmental Toxicology</i> <span>38</span>, no. <span>4</span> (<span>2023</span>): <span>941</span>–<span>949</span>, https://doi.org/10.1002/tox.23739.\u0000 </p><p>The above article, published online on 09 January 2023 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; 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><p>The authors did not respond to communications from the Publisher regarding the retraction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24591","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351795","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}
Benzo[a]pyrene (BaP) is a persistent polycyclic aromatic hydrocarbon (PAH) that poses significant environmental and health risks. Co-metabolic bioremediation, which uses additional carbon sources to enhance microbial degradation, offers a promising approach for BaP removal. This study investigated the effects of different co-metabolic carbon sources on the growth of Achromobacter xylosoxidans B-2 and its efficiency in degrading BaP in both mineral salt medium (MSM) and BaP-contaminated soil. The addition of supplementary carbon sources, particularly starch and salicylic acid, significantly enhanced strain B-2 growth and BaP removal in MSM (p < 0.05), with the highest degradation rate reaching 46.35% in the starch-supplemented group. In soil, salicylic acid and starch also markedly improved BaP degradation, achieving 47.99% and 23.53% removal (both p < 0.01) after 30 days, respectively, compared to only 9.78% in the BaP-only group. Metagenomic analysis revealed that co-substrate amendments significantly altered soil microbiota, enriching PAH-degrading genera such as Achromobacter, especially the introduced A. xylosoxidans. This enrichment was accompanied by reduced overall microbial diversity, indicating strong selective pressure from the amendments. Functional gene profiling based on metagenomic data indicated an increased abundance of key PAH-degrading enzymes, including dioxygenases and dehydrogenases, in response to co-substrate addition. Redundancy analysis further indicated that environmental factors such as pH, organic matter, and phosphorus were significantly correlated with microbial community composition and BaP degradation efficiency. These findings demonstrate that co-metabolism not only enhances BaP removal but also drives functional and ecological changes in soil microbiota, providing mechanistic insight and practical guidance for improved bioremediation strategies.
{"title":"The Co-Metabolic Bioremediation of Benzo[a]pyrene Contaminated Soil by Achromobacter xylosoxidans B-2 and Its Effect on Indigenous Microbial Community.","authors":"Huanhuan Xie,Xinying Zhang,Xiaoyan Liu","doi":"10.1002/tox.24576","DOIUrl":"https://doi.org/10.1002/tox.24576","url":null,"abstract":"Benzo[a]pyrene (BaP) is a persistent polycyclic aromatic hydrocarbon (PAH) that poses significant environmental and health risks. Co-metabolic bioremediation, which uses additional carbon sources to enhance microbial degradation, offers a promising approach for BaP removal. This study investigated the effects of different co-metabolic carbon sources on the growth of Achromobacter xylosoxidans B-2 and its efficiency in degrading BaP in both mineral salt medium (MSM) and BaP-contaminated soil. The addition of supplementary carbon sources, particularly starch and salicylic acid, significantly enhanced strain B-2 growth and BaP removal in MSM (p < 0.05), with the highest degradation rate reaching 46.35% in the starch-supplemented group. In soil, salicylic acid and starch also markedly improved BaP degradation, achieving 47.99% and 23.53% removal (both p < 0.01) after 30 days, respectively, compared to only 9.78% in the BaP-only group. Metagenomic analysis revealed that co-substrate amendments significantly altered soil microbiota, enriching PAH-degrading genera such as Achromobacter, especially the introduced A. xylosoxidans. This enrichment was accompanied by reduced overall microbial diversity, indicating strong selective pressure from the amendments. Functional gene profiling based on metagenomic data indicated an increased abundance of key PAH-degrading enzymes, including dioxygenases and dehydrogenases, in response to co-substrate addition. Redundancy analysis further indicated that environmental factors such as pH, organic matter, and phosphorus were significantly correlated with microbial community composition and BaP degradation efficiency. These findings demonstrate that co-metabolism not only enhances BaP removal but also drives functional and ecological changes in soil microbiota, providing mechanistic insight and practical guidance for improved bioremediation strategies.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"150 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145331647","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}
Exposure to acrylamide (AA) through food is nearly unavoidable and can lead to long-lasting consequences. AA has been shown to cause reproductive toxicity and reduce ovarian weight and follicle number when taken orally. Flavonoids derived from plants are bioactive compounds that are increasingly being used in medicine. In this research, we aimed to investigate the ability of hesperidin (HES), a bioactive compound derived from plants, in shielding rats from AA-induced ovarian damage. We identified possible target genes related to HES therapy and AA toxicity and conducted functional enrichment and pathway analysis to understand their biological significance. Additionally, we performed molecular docking of the core target gene with AA and HES. During the animal experimentation, rats were first exposed to 40 mg/kg of AA orally for 10 days and then received HES therapy at various doses for three consecutive days. All animals were euthanised 24 h after receiving the final treatment. We evaluated reproductive hormones, oxidative stress markers, membrane-bound enzymes, glycogen content, and histological findings to determine the protective efficacy of HES. The study found that HES has a high binding affinity with the core target proteins and showed impressive protection against oxidative damage induced by AA in our in vivo experiment. This protection can likely be attributed to HES's potent antioxidant properties.
{"title":"Hesperidin Attenuates Acrylamide-Induced Ovarian Toxicity in Rats: Based on Network Pharmacology, Molecular Docking, and In Vivo Studies.","authors":"Divya Gupta,Sadhana Shrivastava,Chakresh Kumar Jain,Pankaj Kumar Tripathi,Subodh Kumar,Sangeeta Shukla","doi":"10.1002/tox.24577","DOIUrl":"https://doi.org/10.1002/tox.24577","url":null,"abstract":"Exposure to acrylamide (AA) through food is nearly unavoidable and can lead to long-lasting consequences. AA has been shown to cause reproductive toxicity and reduce ovarian weight and follicle number when taken orally. Flavonoids derived from plants are bioactive compounds that are increasingly being used in medicine. In this research, we aimed to investigate the ability of hesperidin (HES), a bioactive compound derived from plants, in shielding rats from AA-induced ovarian damage. We identified possible target genes related to HES therapy and AA toxicity and conducted functional enrichment and pathway analysis to understand their biological significance. Additionally, we performed molecular docking of the core target gene with AA and HES. During the animal experimentation, rats were first exposed to 40 mg/kg of AA orally for 10 days and then received HES therapy at various doses for three consecutive days. All animals were euthanised 24 h after receiving the final treatment. We evaluated reproductive hormones, oxidative stress markers, membrane-bound enzymes, glycogen content, and histological findings to determine the protective efficacy of HES. The study found that HES has a high binding affinity with the core target proteins and showed impressive protection against oxidative damage induced by AA in our in vivo experiment. This protection can likely be attributed to HES's potent antioxidant properties.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"6 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145305718","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}
Ružica Ždero Pavlović, Denis Uka, Teodora Kukrić, Marina Putnik‐Delić, Ivana Maksimović, Boris M. Popović
Hydrophobic deep eutectic solvents (HDES) have emerged as promising green alternatives to conventional organic solvents, yet their environmental safety remains largely unexplored. This study investigates the phytotoxic effect of five L‐menthol‐based HDES—prepared with caprylic acid, oleic acid, lauric acid, (R)‐(+)‐limonene, and (−)‐α‐pinene—on wheat seeds (Triticum aestivum L.). The individual components and common organic solvents (dimethyl sulfoxide, pyridine, methylene chloride) were also evaluated for comparison. Germination assays revealed that several HDES, particularly those containing oleic acid, limonene, and pinene, exhibited lower phytotoxicity than L‐menthol alone, with germination percentages comparable to control at 0.1 and 0.05 mg/mL. Most treatments significantly increased lipid peroxidation levels, indicating oxidative stress. Additionally, elevated phenylalanine ammonia‐lyase and guaiacol peroxidase activities, along with total phenolic content, suggested activation of antioxidant defense mechanisms. Notably, some HDES induced metabolic shifts without affecting total phenolic content, implying potential redirection of phenylpropanoid metabolism. These findings provide novel insight into the phytotoxic profile of HDES and highlight the importance of assessing their environmental safety prior to agricultural or industrial use.
{"title":"Phytotoxicity of L‐Menthol‐Based Hydrophobic Deep Eutectic Solvents","authors":"Ružica Ždero Pavlović, Denis Uka, Teodora Kukrić, Marina Putnik‐Delić, Ivana Maksimović, Boris M. Popović","doi":"10.1002/tox.24575","DOIUrl":"https://doi.org/10.1002/tox.24575","url":null,"abstract":"Hydrophobic deep eutectic solvents (HDES) have emerged as promising green alternatives to conventional organic solvents, yet their environmental safety remains largely unexplored. This study investigates the phytotoxic effect of five <jats:italic>L</jats:italic>‐menthol‐based HDES—prepared with caprylic acid, oleic acid, lauric acid, (R)‐(+)‐limonene, and (−)‐α‐pinene—on wheat seeds (<jats:styled-content style=\"fixed-case\"><jats:italic>Triticum aestivum</jats:italic></jats:styled-content> L.). The individual components and common organic solvents (dimethyl sulfoxide, pyridine, methylene chloride) were also evaluated for comparison. Germination assays revealed that several HDES, particularly those containing oleic acid, limonene, and pinene, exhibited lower phytotoxicity than <jats:italic>L</jats:italic>‐menthol alone, with germination percentages comparable to control at 0.1 and 0.05 mg/mL. Most treatments significantly increased lipid peroxidation levels, indicating oxidative stress. Additionally, elevated phenylalanine ammonia‐lyase and guaiacol peroxidase activities, along with total phenolic content, suggested activation of antioxidant defense mechanisms. Notably, some HDES induced metabolic shifts without affecting total phenolic content, implying potential redirection of phenylpropanoid metabolism. These findings provide novel insight into the phytotoxic profile of HDES and highlight the importance of assessing their environmental safety prior to agricultural or industrial use.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"21 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145295153","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}
Leila Mohammadi, Tourandokht Baluchnejadmojarad, Mina Goudarzi, Vahid Khodashenas, Mehrdad Roghani
The increasing prevalence of microplastics pollution is a significant environmental challenge. However, the effects of these particles on learning and memory remain poorly understood. The aim of this investigation was to ascertain the influence of miR‐532‐5p on cognitive and memory deficits induced by polystyrene microplastics (PS‐MPs) and to identify the underlying mechanisms. PS‐MPs were administrated orally to male rats at a dose of 30 mg/kg for 8 weeks. In the treatment group, miR‐532‐5p was injected intracerebroventricularly (ICV) at a dose of 2.5 μg/2.5 μL. To assess the effects of PS‐MPs exposure on learning and memory functions, the novel object discrimination (NOD), Y‐maze, and Barnes maze tests were used, which showed a detrimental effect on the subjects' learning and memory abilities. In the hippocampal tissue of the rats exposed to PS‐MPs, the levels of MDA, protein carbonyl, nitrite, TNFα, NLRP3, Caspase 1, caspase 3, and GFAP were increased, and levels of SOD, catalase, SIRT1, and BDNF were decreased. In addition, exposure to PS‐MPs increased AChE activity, activated the PERK/GRP78/CHOP signaling pathway, and inactivated the Wnt/β‐catenin and PI3K/Akt signaling pathways. Conversely, ICV injection of miR‐532‐5p led to a reversal of the hippocampal levels of all aforementioned factors. Therefore, exposure to PS‐MPs can affect learning and memory functions by inducing oxidative stress, neuroinflammation, apoptosis, pyroptosis, and ER stress, and treatment with miR‐532‐5p can restore learning and memory through its anti‐inflammatory, antioxidant, and anti‐pyroptosis properties.
{"title":"MiR‐532‐5p Attenuates Cognitive Deficits and Endoplasmic Reticulum Stress Subsequent to Polystyrene Microplastics","authors":"Leila Mohammadi, Tourandokht Baluchnejadmojarad, Mina Goudarzi, Vahid Khodashenas, Mehrdad Roghani","doi":"10.1002/tox.24569","DOIUrl":"https://doi.org/10.1002/tox.24569","url":null,"abstract":"The increasing prevalence of microplastics pollution is a significant environmental challenge. However, the effects of these particles on learning and memory remain poorly understood. The aim of this investigation was to ascertain the influence of miR‐532‐5p on cognitive and memory deficits induced by polystyrene microplastics (PS‐MPs) and to identify the underlying mechanisms. PS‐MPs were administrated orally to male rats at a dose of 30 mg/kg for 8 weeks. In the treatment group, miR‐532‐5p was injected intracerebroventricularly (ICV) at a dose of 2.5 μg/2.5 μL. To assess the effects of PS‐MPs exposure on learning and memory functions, the novel object discrimination (NOD), Y‐maze, and Barnes maze tests were used, which showed a detrimental effect on the subjects' learning and memory abilities. In the hippocampal tissue of the rats exposed to PS‐MPs, the levels of MDA, protein carbonyl, nitrite, TNFα, NLRP3, Caspase 1, caspase 3, and GFAP were increased, and levels of SOD, catalase, SIRT1, and BDNF were decreased. In addition, exposure to PS‐MPs increased AChE activity, activated the PERK/GRP78/CHOP signaling pathway, and inactivated the Wnt/β‐catenin and PI3K/Akt signaling pathways. Conversely, ICV injection of miR‐532‐5p led to a reversal of the hippocampal levels of all aforementioned factors. Therefore, exposure to PS‐MPs can affect learning and memory functions by inducing oxidative stress, neuroinflammation, apoptosis, pyroptosis, and ER stress, and treatment with miR‐532‐5p can restore learning and memory through its anti‐inflammatory, antioxidant, and anti‐pyroptosis properties.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"3 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282992","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}
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