Toxics

Editorial

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4 pages, 172 KiB

Open AccessEditorial

Environmental Chemical Exposomics and Metabolomics in Toxicology: The Latest Updates

by Minjian Chen

Toxics 2024, 12(9), 647; https://doi.org/10.3390/toxics12090647 - 4 Sep 2024

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Abstract

This Editorial introduces the Special Issue titled “State-of-the-Art Environmental Chemical Exposomics and Metabolomics” [...] Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

Research

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14 pages, 2061 KiB

Open AccessArticle

Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells

by Chengzhi Liu, Shuang Chen, Jiangliang Chu, Yifan Yang, Beilei Yuan and Huazhong Zhang

Toxics 2024, 12(6), 399; https://doi.org/10.3390/toxics12060399 - 30 May 2024

Cited by 1 | Viewed by 1729

Abstract

Polyvinyl chloride microplastics (PVC-MPs) are microplastic pollutants widely present in the environment, but their potential risks to human lung health and underlying toxicity mechanisms remain unknown. In this study, we systematically analyzed the effects of PVC-MPs on the transcriptome and metabolome of BEAS-2B [...] Read more.

Polyvinyl chloride microplastics (PVC-MPs) are microplastic pollutants widely present in the environment, but their potential risks to human lung health and underlying toxicity mechanisms remain unknown. In this study, we systematically analyzed the effects of PVC-MPs on the transcriptome and metabolome of BEAS-2B cells using high-throughput RNA sequencing and untargeted metabolomics technologies. The results showed that exposure to PVC-MPs significantly reduced the viability of BEAS-2B cells, leading to the differential expression of 530 genes and 3768 metabolites. Further bioinformatics analyses showed that PVC-MP exposure influenced the expression of genes associated with fluid shear stress, the MAPK and TGF-β signaling pathways, and the levels of metabolites associated with amino acid metabolism. In particular, integrated pathway analysis showed that lipid metabolic pathways (including glycerophospholipid metabolism, glycerolipid metabolism, and sphingolipid metabolism) were significantly perturbed in BEAS-2B cells following PVC-MPs exposure. This study provides new insights and targets for a deeper understanding of the toxicity mechanism of PVC-MPs and for the prevention and treatment of PVC-MP-associated lung diseases. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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19 pages, 3347 KiB

Open AccessArticle

High-Coverage UHPLC-MS/MS Analysis of 67 Mycotoxins in Plasma for Male Infertility Exposure Studies

by Xiao Ning, Lulu Wang, Jia-Sheng Wang, Jian Ji, Shaoming Jin, Jiadi Sun, Yongli Ye, Shenghui Mei, Yinzhi Zhang, Jin Cao and Xiulan Sun

Toxics 2024, 12(6), 395; https://doi.org/10.3390/toxics12060395 - 28 May 2024

Cited by 1 | Viewed by 1103

Abstract

Mycotoxins are a class of exogenous metabolites that are major contributors to foodborne diseases and pose a potential threat to human health. However, little attention has been paid to trace mycotoxin co-exposure situations in vivo. To address this, we devised a novel analytical [...] Read more.

Mycotoxins are a class of exogenous metabolites that are major contributors to foodborne diseases and pose a potential threat to human health. However, little attention has been paid to trace mycotoxin co-exposure situations in vivo. To address this, we devised a novel analytical strategy, both highly sensitive and comprehensive, for quantifying 67 mycotoxins in human plasma samples. This method employs isotope dilution mass spectrometry (IDMS) for approximately 40% of the analytes and utilizes internal standard quantification for the rest. The mycotoxins were classified into three categories according to their physicochemical properties, facilitating the optimization of extraction and detection parameters to improve analytical performance. The lowest limits of detection and quantitation were 0.001–0.5 μg/L and 0.002–1 μg/L, respectively, the intra-day precision ranged from 1.8% to 11.9% RSD, and the intra-day trueness ranged from 82.7–116.6% for all mycotoxins except Ecl, DH-LYS, PCA, and EnA (66.4–129.8%), showing good analytical performance of the method for biomonitoring. A total of 40 mycotoxins (including 24 emerging mycotoxins) were detected in 184 plasma samples (89 from infertile males and 95 from healthy males) using the proposed method, emphasizing the widespread exposure of humans to both traditional and emerging mycotoxins. The most frequently detected mycotoxins were ochratoxin A, ochratoxin B, enniatin B, and citrinin. The incidence of exposure to multiple mycotoxins was significantly higher in infertile males than in healthy subjects, particularly levels of ochratoxin A, ochratoxin B, and citrinin, which were significantly increased. It is necessary to carry out more extensive biological monitoring to provide data support for further study of the relationship between mycotoxins and male infertility. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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14 pages, 5253 KiB

Open AccessArticle

Inhibitory Impact of Prenatal Exposure to Nano-Polystyrene Particles on the MAP2K6/p38 MAPK Axis Inducing Embryonic Developmental Abnormalities in Mice

by Junyi Lv, Qing He, Zixiang Yan, Yuan Xie, Yao Wu, Anqi Li, Yuqing Zhang, Jing Li and Zhenyao Huang

Toxics 2024, 12(5), 370; https://doi.org/10.3390/toxics12050370 - 17 May 2024

Viewed by 1380

Abstract

Nanoplastics, created by the fragmentation of larger plastic debris, are a serious pollutant posing substantial environmental and health risks. Here, we developed a polystyrene nanoparticle (PS-NP) exposure model during mice pregnancy to explore their effects on embryonic development. We found that exposure to [...] Read more.

Nanoplastics, created by the fragmentation of larger plastic debris, are a serious pollutant posing substantial environmental and health risks. Here, we developed a polystyrene nanoparticle (PS-NP) exposure model during mice pregnancy to explore their effects on embryonic development. We found that exposure to 30 nm PS-NPs during pregnancy resulted in reduced mice placental weight and abnormal embryonic development. Subsequently, our transcriptomic dissection unveiled differential expression in 102 genes under PS-NP exposure and the p38 MAPK pathway emerged as being significantly altered in KEGG pathway mapping. Our findings also included a reduction in the thickness of the trophoblastic layer in the placenta, diminished cell invasion capabilities, and an over-abundance of immature red cells in the blood vessels of the mice. In addition, we validated our findings through the human trophoblastic cell line, HTR-8/SVneo (HTR). PS-NPs induced a drop in the vitality and migration capacities of HTR cells and suppressed the p38 MAPK signaling pathway. This research highlights the embryotoxic effects of nanoplastics on mice, while the verification results from the HTR cells suggest that there could also be certain impacts on the human trophoblast layer, indicating a need for further exploration in this area. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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15 pages, 14887 KiB

Open AccessArticle

Titanium Dioxide Nanoparticles Induce Maternal Preeclampsia-like Syndrome and Adverse Birth Outcomes via Disrupting Placental Function in SD Rats

by Haixin Li, Dandan Miao, Haiting Hu, Pingping Xue, Kun Zhou and Zhilei Mao

Toxics 2024, 12(5), 367; https://doi.org/10.3390/toxics12050367 - 16 May 2024

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Abstract

The escalating utilization of titanium dioxide nanoparticles (TiO₂ NPs) in everyday products has sparked concerns regarding their potential hazards to pregnant females and their offspring. To address these concerns and shed light on their undetermined adverse effects and mechanisms, we established a [...] Read more.

The escalating utilization of titanium dioxide nanoparticles (TiO₂ NPs) in everyday products has sparked concerns regarding their potential hazards to pregnant females and their offspring. To address these concerns and shed light on their undetermined adverse effects and mechanisms, we established a pregnant rat model to investigate the impacts of TiO₂ NPs on both maternal and offspring health and to explore the underlying mechanisms of those impacts. Pregnant rats were orally administered TiO₂ NPs at a dose of 5 mg/kg body weight per day from GD5 to GD18 during pregnancy. Maternal body weight, organ weight, and birth outcomes were monitored and recorded. Maternal pathological changes were examined by HE staining and TEM observation. Maternal blood pressure was assessed using a non-invasive blood analyzer, and the urinary protein level was determined using spot urine samples. Our findings revealed that TiO₂ NPs triggered various pathological alterations in maternal liver, kidney, and spleen, and induced maternal preeclampsia-like syndrome, as well as leading to growth restriction in the offspring. Further examination unveiled that TiO₂ NPs hindered trophoblastic cell invasion into the endometrium via the promotion of autophagy. Consistent hypertension and proteinuria resulted from the destroyed the kidney GBM. In total, an exposure to TiO₂ NPs during pregnancy might increase the risk of human preeclampsia through increased maternal arterial pressure and urinary albumin levels, as well as causing fetal growth restriction in the offspring. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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19 pages, 2084 KiB

Open AccessArticle

Restricted-Access Media Column Switching Online Solid-Phase Extraction UHPLC–MS/MS for the Determination of Seven Type B Trichothecenes in Whole-Grain Preprocessed Foods and Human Exposure Risk Assessment

by Xiao Ning, Yongli Ye, Jian Ji, Yanchun Hui, Jingyun Li, Po Chen, Shaoming Jin, Tongtong Liu, Yinzhi Zhang, Jin Cao and Xiulan Sun

Toxics 2024, 12(5), 336; https://doi.org/10.3390/toxics12050336 - 6 May 2024

Viewed by 1259

Abstract

With increasing health awareness and the accelerating pace of life, whole-grain prepared foods have gained popularity due to their health benefits and convenience. However, the potential risk of type B trichothecene toxins has also increased, and these mycotoxins in such foods are rarely [...] Read more.

With increasing health awareness and the accelerating pace of life, whole-grain prepared foods have gained popularity due to their health benefits and convenience. However, the potential risk of type B trichothecene toxins has also increased, and these mycotoxins in such foods are rarely regulated. In this study, a quantitative method combining a single-valve dual-column automatic online solid-phase extraction system with ultra-high-performance liquid chromatography–tandem mass spectrometry (UHPLC–MS/MS) was developed for the first time using restricted-access media columns. This method can simultaneously determine trace residues of seven type B trichothecenes within 15 min. The method is convenient, sensitive (limit of detection and quantification of 0.05–0.6 μg/kg and 0.15–2 μg/kg, respectively), accurate (recovery rates of 90.3%–106.6%, relative standard deviation < 4.3%), and robust (>1000 times). The established method was applied to 160 prepared food samples of eight categories sold in China. At least one toxin was detected in 70% of the samples. Whole-wheat dumpling wrappers had the highest contamination rate (95%) and the highest total content of type B trichothecenes in a single sample (2077.3 μg/kg). Exposure risk assessment indicated that the contamination of whole-grain prepared foods has been underestimated. The total health risk index of whole-wheat dumpling wrappers, which are susceptible to deoxynivalenol, reached 136.41%, posing a significant threat to human health. Effective measures urgently need to be taken to control this risk. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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15 pages, 2010 KiB

Open AccessEditor’s ChoiceArticle

Exposure to Molybdate Results in Metabolic Disorder: An Integrated Study of the Urine Elementome and Serum Metabolome in Mice

by Kun Zhou, Miaomiao Tang, Wei Zhang, Yanling Chen, Yusheng Guan, Rui Huang, Jiawei Duan, Zibo Liu, Xiaoming Ji, Yingtong Jiang, Yanhui Hu, Xiaoling Zhang, Jingjing Zhou and Minjian Chen

Toxics 2024, 12(4), 288; https://doi.org/10.3390/toxics12040288 - 14 Apr 2024

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Abstract

The increasing use of molybdate has raised concerns about its potential toxicity in humans. However, the potential toxicity of molybdate under the current level of human exposure remains largely unknown. Endogenous metabolic alterations that are caused in humans by environmental exposure to pollutants [...] Read more.

The increasing use of molybdate has raised concerns about its potential toxicity in humans. However, the potential toxicity of molybdate under the current level of human exposure remains largely unknown. Endogenous metabolic alterations that are caused in humans by environmental exposure to pollutants are associated with the occurrence and progression of many diseases. This study exposed eight-week-old male C57 mice to sodium molybdate at doses relevant to humans (0.01 and 1 mg/kg/day) for eight weeks. Inductively coupled plasma mass spectrometry (ICP-MS) and ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS) were utilized to assess changes in urine element levels and serum metabolites in mice, respectively. A total of 838 subjects from the NHANES 2017–2018 population database were also included in our study to verify the associations between molybdenum and cadmium found in mice. Analysis of the metabolome in mice revealed that four metabolites in blood serum exhibited significant changes, including 5-aminolevulinic acid, glycolic acid, l-acetylcarnitine, and 2,3-dihydroxypropyl octanoate. Analysis of the elementome revealed a significant increase in urine levels of cadmium after molybdate exposure in mice. Notably, molybdenum also showed a positive correlation with cadmium in humans from the NHANES database. Further analysis identified a positive correlation between cadmium and 2,3-dihydroxypropyl octanoate in mice. In conclusion, these findings suggest that molybdate exposure disrupted amino acid and lipid metabolism, which may be partially mediated by molybdate-altered cadmium levels. The integration of elementome and metabolome data provides sensitive information on molybdate-induced metabolic disorders and associated toxicities at levels relevant to human exposure. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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17 pages, 1977 KiB

Open AccessFeature PaperEditor’s ChoiceArticle

A Metabolome and Microbiome Analysis of Acute Myeloid Leukemia: Insights into the Carnosine–Histidine Metabolic Pathway

by Binxiong Wu, Yuntian Xu, Miaomiao Tang, Yingtong Jiang, Ting Zhang, Lei Huang, Shuyang Wang, Yanhui Hu, Kun Zhou, Xiaoling Zhang and Minjian Chen

Toxics 2024, 12(1), 14; https://doi.org/10.3390/toxics12010014 - 22 Dec 2023

Cited by 1 | Viewed by 2025

Abstract

Metabolism underlies the pathogenesis of acute myeloid leukemia (AML) and can be influenced by gut microbiota. However, the specific metabolic changes in different tissues and the role of gut microbiota in AML remain unclear. In this study, we analyzed the metabolome differences in [...] Read more.

Metabolism underlies the pathogenesis of acute myeloid leukemia (AML) and can be influenced by gut microbiota. However, the specific metabolic changes in different tissues and the role of gut microbiota in AML remain unclear. In this study, we analyzed the metabolome differences in blood samples from patients with AML and healthy controls using UPLC-Q-Exactive. Additionally, we examined the serum, liver, and fecal metabolome of AML model mice and control mice using UPLC-Q-Exactive. The gut microbiota of the mice were analyzed using 16S rRNA sequencing. Our UPLC-MS analysis revealed significant differences in metabolites between the AML and control groups in multiple tissue samples. Through cross-species validation in humans and animals, as well as reverse validation of Celastrol, we discovered that the Carnosine–Histidine metabolic pathway may play a potential role in the occurrence and progression of AML. Furthermore, our analysis of gut microbiota showed no significant diversity changes, but we observed a significant negative correlation between the key metabolite Carnosine and Peptococcaceae and Campylobacteraceae. In conclusion, the Carnosine–Histidine metabolic pathway influences the occurrence and progression of AML, while the gut microbiota might play a role in this process. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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10 pages, 2402 KiB

Open AccessEditor’s ChoiceArticle

The Cytotoxicity of Tungsten Ions Derived from Nanoparticles Correlates with Pulmonary Toxicity

by Jun Yao, Pengfei Zhou, Xin Zhang, Beilei Yuan, Yong Pan and Juncheng Jiang

Toxics 2023, 11(6), 528; https://doi.org/10.3390/toxics11060528 - 13 Jun 2023

Cited by 1 | Viewed by 1768

Abstract

Tungsten carbide nanoparticles (nano-WC) are prevalent in composite materials, and are attributed to their physical and chemical properties. Due to their small size, nano-WC particles can readily infiltrate biological organisms via the respiratory tract, thereby posing potential health hazards. Despite this, the studies [...] Read more.

Tungsten carbide nanoparticles (nano-WC) are prevalent in composite materials, and are attributed to their physical and chemical properties. Due to their small size, nano-WC particles can readily infiltrate biological organisms via the respiratory tract, thereby posing potential health hazards. Despite this, the studies addressing the cytotoxicity of nano-WC remain notably limited. To this purpose, the BEAS-2B and U937 cells were cultured in the presence of nano-WC. The significant cytotoxicity of nano-WC suspension was evaluated using a cellular LDH assay. To investigate the cytotoxic impact of tungsten ions (W⁶⁺) on cells, the ion chelator (EDTA-2Na) was used to adsorb W⁶⁺ from nano-WC suspension. Subsequent to this treatment, the modified nano-WC suspension was subjected to flow cytometry analysis to evaluate the rates of cellular apoptosis. According to the results, a decrease in W⁶⁺ could mitigate the cellular damage and enhance cell viability, which indicated that W⁶⁺ indeed exerted a significant cytotoxic influence on the cells. Overall, the present study provides valuable insight into the toxicological mechanisms underlying the exposure of lung cells to nano-WC, thereby reducing the environmental toxicant risk to human health. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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15 pages, 3952 KiB

Open AccessArticle

Cigarette Smoke-Induced Gastric Cancer Cell Exosomes Affected the Fate of Surrounding Normal Cells via the Circ0000670/Wnt/β-Catenin Axis

by Zhaofeng Liang, Shikun Fang, Yue Zhang, Xinyi Zhang, Yumeng Xu, Hui Qian and Hao Geng

Toxics 2023, 11(5), 465; https://doi.org/10.3390/toxics11050465 - 17 May 2023

Cited by 2 | Viewed by 1866

Abstract

Cigarette smoke is a major risk factor for gastric cancer. Exosomes are an important part of intercellular and intra-organ communication systems and can carry circRNA and other components to play a regulatory role in the occurrence and development of gastric cancer. However, it [...] Read more.

Cigarette smoke is a major risk factor for gastric cancer. Exosomes are an important part of intercellular and intra-organ communication systems and can carry circRNA and other components to play a regulatory role in the occurrence and development of gastric cancer. However, it is unclear whether cigarette smoke can affect exosomes and exosomal circRNA to promote the development of gastric cancer. Exosomes secreted by cancer cells promote cancer development by affecting surrounding normal cells. Herein, we aimed to clarify whether the exosomes secreted by cigarette smoke-induced gastric cancer cells can promote the development of gastric cancer by affecting the surrounding gastric mucosal epithelial cells (GES-1). In the present study, we treated gastric cancer cells with cigarette smoke extract for 4 days and demonstrated that cigarette smoke promotes the stemness and EMT of gastric cancer cells and cigarette smoke-induced exosomes promote stemness gene expression, EMT processes and the proliferation of GES-1 cells. We further found that circ0000670 was up-regulated in tissues of gastric cancer patients with smoking history, cigarette smoke-induced gastric cancer cells and their exosomes. Functional assays showed that circ0000670 knockdown inhibited the promoting effects of cigarette smoke-induced exosomes on the stemness and EMT characteristic of GES-1 cells, whereas its overexpression had the opposite effect. In addition, exosomal circ0000670 was found to promote the development of gastric cancer by regulating the Wnt/β-catenin pathway. Our findings indicated that exosomal circ0000670 promotes cigarette smoke-induced gastric cancer development, which might provide a new basis for the treatment of cigarette smoke-related gastric cancer. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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12 pages, 4941 KiB

Open AccessArticle

Multi-Omics Analyses Reveal the Mechanisms of Early Stage Kidney Toxicity by Diquat

by Huazhong Zhang, Jinsong Zhang, Jinquan Li, Zhengsheng Mao, Jian Qian, Cheng Zong, Hao Sun and Beilei Yuan

Toxics 2023, 11(2), 184; https://doi.org/10.3390/toxics11020184 - 16 Feb 2023

Cited by 8 | Viewed by 2399

Abstract

Diquat (DQ), a widely used bipyridyl herbicide, is associated with significantly higher rates of kidney injuries compared to other pesticides. However, the underlying molecular mechanisms are largely unknown. In this study, we identified the molecular changes in the early stage of DQ-induced kidney [...] Read more.

Diquat (DQ), a widely used bipyridyl herbicide, is associated with significantly higher rates of kidney injuries compared to other pesticides. However, the underlying molecular mechanisms are largely unknown. In this study, we identified the molecular changes in the early stage of DQ-induced kidney damage in a mouse model through transcriptomic, proteomic and metabolomic analyses. We identified 869 genes, 351 proteins and 96 metabolites that were differentially expressed in the DQ-treated mice relative to the control mice (p < 0.05), and showed significant enrichment in the PPAR signaling pathway and fatty acid metabolism. Hmgcs2, Cyp4a10, Cyp4a14 and Lpl were identified as the major proteins/genes associated with DQ-induced kidney damage. In addition, eicosapentaenoic acid, linoleic acid, palmitic acid and (R)-3-hydroxybutyric acid were the major metabolites related to DQ-induced kidney injury. Overall, the multi-omics analysis showed that DQ-induced kidney damage is associated with dysregulation of the PPAR signaling pathway, and an aberrant increase in Hmgcs2 expression and 3-hydroxybutyric acid levels. Our findings provide new insights into the molecular basis of DQ-induced early kidney damage. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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17 pages, 3724 KiB

Open AccessEditor’s ChoiceArticle

Stage-Related Neurotoxicity of BPA in the Development of Zebrafish Embryos

by Jianjun Liu, Wenyu Kong, Yuchen Liu, Qiyao Ma, Qi Shao, Liwen Zeng, Yu Chao, Xiaoyao Song and Jie Zhang

Toxics 2023, 11(2), 177; https://doi.org/10.3390/toxics11020177 - 14 Feb 2023

Cited by 7 | Viewed by 2408

Abstract

Bisphenol A (BPA) is one of the most widely produced chemicals in the world used in the production of epoxy resins and polycarbonate plastics. BPA is easily migrated from the outer packaging to the contents. Due to the lipophilic property, BPA is easily [...] Read more.

Bisphenol A (BPA) is one of the most widely produced chemicals in the world used in the production of epoxy resins and polycarbonate plastics. BPA is easily migrated from the outer packaging to the contents. Due to the lipophilic property, BPA is easily accumulated in organisms. Perinatal low-dose BPA exposure alters brain neural development in later generations. In this study, after BPA treatment, the spontaneous movement of zebrafish larvae from the cleavage period to the segmentation period (1–24 hpf) was significantly decreased, with speed decreasing by 18.97% and distance decreasing between 18.4 and 29.7% compared to controls. Transcriptomics analysis showed that 131 genes were significantly differentially expressed in the exposed group during the 1–24 hpf period, among which 39 genes were significantly upregulated and 92 genes were significantly downregulated. The GO enrichment analysis, gene function analysis and real-time quantitative PCR of differentially expressed genes showed that the mRNA level of guanine deaminase (cypin) decreased significantly in the 1–24 hpf period. Moreover, during the 1–24 hpf period, BPA exposure reduced guanine deaminase activity. Therefore, we confirmed that cypin is a key sensitive gene for BPA during this period. Finally, the cypin mRNA microinjection verified that the cypin level of zebrafish larvae was restored, leading to the restoration of the locomotor activity. Taken together, the current results show that the sensitive period of BPA to zebrafish embryos is from the cleavage period to the segmentation period (1–24 hpf), and cypin is a potential target for BPA-induced neurodevelopmental toxicity. This study provides a potential sensitive period and a potential target for the deep understanding of neurodevelopmental toxicity mechanisms caused by BPA. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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11 pages, 1633 KiB

Open AccessArticle

A UPLC Q-Exactive Orbitrap Mass Spectrometry-Based Metabolomic Study of Serum and Tumor Tissue in Patients with Papillary Thyroid Cancer

by Bo Xu, Wei Gao, Ting Xu, Cuiping Liu, Dan Wu and Wei Tang

Toxics 2023, 11(1), 44; https://doi.org/10.3390/toxics11010044 - 31 Dec 2022

Cited by 2 | Viewed by 2259

Abstract

Objective: To find the metabolomic characteristics of tumor or para-tumor tissues, and the differences in serums from papillary thyroid cancer (PTC) patients with or without lymph node metastasis. Methods: We collected serums of PTC patients with/without lymph node metastasis (SN1/SN0), tumor and adjacent [...] Read more.

Objective: To find the metabolomic characteristics of tumor or para-tumor tissues, and the differences in serums from papillary thyroid cancer (PTC) patients with or without lymph node metastasis. Methods: We collected serums of PTC patients with/without lymph node metastasis (SN1/SN0), tumor and adjacent tumor tissues of PTC patients with lymph node metastasis (TN1 and PN1), and without lymph node metastasis (TN0 and PN0). Metabolite detection was performed by ultra-high performance liquid chromatography combined with Q-Exactive orbitrap mass spectrometry (UPLC Q-Exactive). Results: There were 31, 15, differential metabolites in the comparisons of TN1 and PN1, TN0 and PN0, respectively. Seven uniquely increased metabolites and fourteen uniquely decreased metabolites appeared in the lymph node metastasis (TN1 and PN1) group. Meanwhile, the results indicated that four pathways were co-owned pathways in two comparisons (TN1 and PN1, TN0 and PN0), and four unique pathways presented in the lymph node metastasis (TN1 and PN1) group. Conclusions: Common or differential metabolites and metabolic pathways were detected in the lymph node metastasis and non-metastatic group, which might provide novel ways for the diagnosis and treatment of PTC. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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15 pages, 860 KiB

Open AccessReview

Progress in Research on the Role of the Thioredoxin System in Chemical Nerve Injury

by Xinwei Xu, Lan Zhang, Yuyun He, Cong Qi and Fang Li

Toxics 2024, 12(7), 510; https://doi.org/10.3390/toxics12070510 - 15 Jul 2024

Viewed by 1042

Abstract

(1) Background: Various factors, such as oxidative stress, mitochondrial dysfunction, tumors, inflammation, trauma, immune disorders, and neuronal toxicity, can cause nerve damage. Chemical nerve injury, which results from exposure to toxic chemicals, has garnered increasing research attention. The thioredoxin (Trx) system, comprising Trx, [...] Read more.

(1) Background: Various factors, such as oxidative stress, mitochondrial dysfunction, tumors, inflammation, trauma, immune disorders, and neuronal toxicity, can cause nerve damage. Chemical nerve injury, which results from exposure to toxic chemicals, has garnered increasing research attention. The thioredoxin (Trx) system, comprising Trx, Trx reductase, nicotinamide adenine dinucleotide phosphate, and Trx-interacting protein (TXNIP; endogenous Trx inhibitor), helps maintain redox homeostasis in the central nervous system. The dysregulation of this system can cause dementia, cognitive impairment, nerve conduction disorders, movement disorders, and other neurological disorders. Thus, maintaining Trx system homeostasis is crucial for preventing or treating nerve damage. (2) Objective: In this review study, we explored factors influencing the homeostasis of the Trx system and the involvement of its homeostatic imbalance in chemical nerve injury. In addition, we investigated the therapeutic potential of the Trx system-targeting active substances against chemical nerve injury. (3) Conclusions: Chemicals such as morphine, metals, and methylglyoxal interfere with the activity of TXNIP, Trx, and Trx reductase, disrupting Trx system homeostasis by affecting the phosphatidylinositol-3-kinase/protein kinase B, extracellular signal-regulated kinase, and apoptotic signaling-regulated kinase 1/p38 mitogen-activated protein kinase pathways, thereby leading to neurological disorders. Active substances such as resveratrol and lysergic acid sulfide mitigate the symptoms of chemical nerve injury by regulating the Ras/Raf1/extracellular signal-regulated kinase pathway and the miR-146a-5p/TXNIP axis. This study may guide the development of Trx-targeting modulators for treating neurological disorders and chemical nerve injuries. Full article

(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)

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