Environmental Toxicology最新文献

RETRACTION: J. Sun, Y. Li, R. Chen, Y. Xie, J. Wei, and B. Li, “ Exploring the Role of Lactylation-Related Genes in Osteosarcoma: A Deep Dive into Prognostic Significance and Therapeutic Potential,” Environmental Toxicology 39, no. 2 (2023): 1001–1017, https://doi.org/10.1002/tox.24011.

The above article, published online on 27 November 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC.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.

Retraction: J. Fang, C. Shi, Q. Huang, L. Huang, X. Wang, and B. Yan, "Development of the ARDS-Derived Gene Panel for Lung Adenocarcinoma Prognosis Stratification and Experiment Validation of CCL20 Expression," Environmental Toxicology 39, no. 5 (2024): 3211-3224, https://doi.org/10.1002/tox.24161. The above article, published online on 14 February 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC.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 Biqing Yan disagrees with this decision. The other authors did not respond.

RETRACTION: C. Qu, Q. Wu, J. Lu, and F. Li, “ Prognostic Value and Potential Mechanism of Cellular Senescence and Tumor Microenvironment in Hepatocellular Carcinoma: Insights from Bulk Transcriptomics and Single-Cell Sequencing Analysis,” Environmental Toxicology 39, no. 5 (2024): 2512–2527, https://doi.org/10.1002/tox.24121.

The above article, published online on 08 January 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC.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.

RETRACTION: J. Lu, Y. Feng, Y. Zhou, Z. Xiao, Z. Yang, J. Li, H. Cai, and J. Wang, “ DPM2 Serve as Novel Oncogene and Prognostic Marker Transactivated by ESR1 in Breast Cancer,” Environmental Toxicology 39, no. 3 (2024): 1737–1746, https://doi.org/10.1002/tox.24059.

The above article, published online on 05 December 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; 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 Jie Wang disagrees with this decision. The other authors did not respond.

Retraction: Y. Meng, C. Zhang, T. Fu, J. He, J. Wu, and Y. Zhan, “ Exploring the Tumor Microenvironment: Chemokine-Related Genes and Immunotherapy/Chemotherapy Response in Clear-Cell Renal Cell Carcinoma,” Environmental Toxicology (EarlyView): https://doi.org/10.1002/tox.24190.

The above article, published online on 15 March 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; 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.

RETRACTION: Z. Ni, W. Liu, G. Pan, A. Mao, J. Liu, Q. Zhang, J. Li, L. Liu, and H. Li, “ Circular Forms of Dedicator of Cytokinesis 1 Promotes Breast Cancer Progression by Derepressing Never in Mitosis Related Kinase 2 via Sponging miR-128-3p,” Environmental Toxicology 38, no. 7 (2023): 1712–1722, https://doi.org/10.1002/tox.23799.

The above article, published online on 11 April 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; 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.

Clothianidin (CLO) is a high-frequently detected neonicotinoid pesticide in fruits and vegetables, whose exposure security deserves attention. This study evaluated the apoptotic toxicity of CLO on Caco-2 cells at doses of 100 nM, 10 μM, and 1 mM. After exposure, CLO induced to a remarkable change of signaling proteins that participated in the process of cell apoptosis, including caspase 3, cleaved-caspase 3, and caspase 9. CLO treatment further induced a decrease of mitochondrial membrane potential and increased the protein level of cytochrome C. Reactive oxygen species (ROS) and intracellular Ca²⁺ were also found elevated, indicating an oxidative damage caused by CLO treatment. Moreover, the production of ROS occurred in advance of Ca²⁺ elevation, since inhibiting ROS production could recover the elevation of Ca²⁺ induced by CLO exposure. The protein level of metabolic enzyme cytochrome P450 3A4 (CYP3A4) was downregulated after the treatment of CLO. Molecular docking simulation indicated that CLO had good binding characteristics with CYP3A4. Amino acid sites Arg105, Arg130, and Leu373 in CYP3A4, and nitro group and chlorothiazole group in CLO structure might be the potential binding action target. These results indicated that CLO exposure could induce an apoptotic effect on Caco-2 cells, possibly acting through combining and inhibiting its metabolic enzyme CYP3A4, and then leading to oxidative stress and mitochondrial damage. Thus, CLO exposure might be a potential risk factor for human intestinal health.

The increasing incidence of cancer underscore the necessity of investigating contributors such as endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA). Although BPA's risks are well-documented, comprehensive studies on its substitutes, such as bisphenol B (BPB), are limited. Dysregulated lipid metabolism is a hallmark of cancer progression. Our previous work demonstrated that BPA and bisphenol S (BPS) disrupt lipid metabolism via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. We hence hypothesized that BPB might similarly perturb lipid metabolism and promote tumor growth. BPB's impact on lipid metabolism was investigated in vitro and in vivo using B16 melanoma cancer cells. Our findings indicate BPB exposure significantly increased lipid metabolism in B16 cells, enhancing cell proliferation and migration, and promoting tumor development in mice. Utilizing siRNA transfection or chemical inhibitor, we found that stearoyl-CoA desaturase-1 (SCD1), a key enzyme in lipid synthesis pathway, was required for BPB-induced lipid accumulation and cancer cell migration. Docking analysis revealed BPB may activate gene expression related to lipid metabolism and angiogenesis by interacting with PPARγ and hypoxia-inducible factor-1α (HIF-1α). This study illuminates BPB's potential role in advancing melanoma through lipid metabolism manipulation, highlighting the need for further research into the safety of BPA substitutes and their impact on cancer development.

This study aimed to report the effects of chronic exposure of zebrafish exposed to environmentally relevant concentrations of 0.5, 2.4, and 5.0 mg L^-1 iron (Fe) and 0.2, 0.4, and 2.0 mg L^-1 aluminum (Al). We also evaluated the reversal and generational transposition (F1) of possible histopathological, behavioral, and genotoxic changes in the species. Locomotion changes that may have been caused by the increase in the number of apoptotic cells and in the telencephalic mitochondrial activity were observed especially after the 30 days exposure to Al and persisted after recovery (30 days). We also observed histopathological changes, such as an increase in the number of intestinal goblet cells, even after the recovery period in these animals. Our results also showed that the Fe concentrations used were insufficient to cause genotoxicity, behavioral and intestinal epithelium changes. The adult offspring (F1) of animals exposed to Al showed changes in locomotion and in the amount of goblet cells, demonstrating that even in low concentrations this pollutant can harm subsequent generations in the aquatic biota. Animals demonstrate, in general, greater tolerance to Fe which may be related to the physiological demand of this metal by the body. Even so, all concentrations of both metals that caused some change in the species represent Brazilian environmental occurrences or Brazilian legislation. It highlights the need for updating the guidelines and constant monitoring of aquatic environments, since even in the face of a hypothetical decontamination of the environment, some changes could persist and affect different trophic levels.