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Article ; Online: The potential health risks of N,N-dimethylformamide: An updated review.

Hong, Shu-Jun / Zhang, Xiu-Ning / Sun, Zhan / Zeng, Tao

2024

Abstract: N,N-dimethylformamide (DMF) is a universally used industrial material with exponential growth in production and consumption worldwide. The frequently reported occupational DMF poisoning cases in some countries and the gradually recognized unavoidable ... ...

Abstract	N,N-dimethylformamide (DMF) is a universally used industrial material with exponential growth in production and consumption worldwide. The frequently reported occupational DMF poisoning cases in some countries and the gradually recognized unavoidable health risks to the general population highlight that DMF should still be a matter of concern. Previous studies have demonstrated that the liver is the primary target organ of DMF exposure and multiple mechanisms have been revealed. However, most of these studies investigate the detrimental effects of acute and subacute DMF exposure, while the effects of chronic DMF exposure are rarely studied. Furthermore, the key mechanism for the acute hepatotoxicity of DMF remains to be elucidated. Future research may focus on the identification of efficient preventive measures against the toxicity of DMF to occupational workers, the investigation of the detrimental effects of DMF at environmentally relevant doses, and the studies on the elimination and recycling of DMF in industrial wastes. Herein, we present an updated review of the metabolism of DMF, the biomarker of DMF exposure, underlying molecular mechanisms of DMF-induced hepatotoxicity, and the toxicity of DMF to both occupational workers and general populations and discuss the possible directions in future studies.
Language	English
Publishing date	2024-02-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	604625-3
ISSN	1099-1263 ; 0260-437X
ISSN (online)	1099-1263
ISSN	0260-437X
DOI	10.1002/jat.4590
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Zs.A 1661: Show issues

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Article ; Online: NLRP3 inflammasome activation triggers severe inflammatory liver injury in N, N-dimethylformamide-exposed mice.

Zhang, Xiu-Ning / Zhang, Yan-Jing / Wang, Lin / Hong, Shu-Jun / Zhang, Cui-Li / Zhao, Xiu-Lan / Zeng, Tao

The Science of the total environment

2024 Volume 929, Page(s) 172653

Abstract: N,N-dimethylformamide (DMF) is a widely utilized chemical solvent with various industrial applications. Previous studies have indicated that the liver is the most susceptible target to DMF exposure, whereas the underlying mechanisms remain to be ... ...

Abstract	N,N-dimethylformamide (DMF) is a widely utilized chemical solvent with various industrial applications. Previous studies have indicated that the liver is the most susceptible target to DMF exposure, whereas the underlying mechanisms remain to be elucidated. This study aimed to investigate the role of NLRP3 inflammasome in DMF-induced liver injury in mice by using two NLRP3 inflammasome inhibitors, Nlrp3
MeSH term(s)	Animals ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Mice ; Inflammasomes/metabolism ; Dimethylformamide ; Chemical and Drug Induced Liver Injury ; Liver/drug effects ; Mice, Knockout ; Endoplasmic Reticulum Stress/drug effects
Chemical Substances	NLR Family, Pyrin Domain-Containing 3 Protein ; Inflammasomes ; Dimethylformamide (8696NH0Y2X) ; Nlrp3 protein, mouse
Language	English
Publishing date	2024-04-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	121506-1
ISSN	1879-1026 ; 0048-9697
ISSN (online)	1879-1026
ISSN	0048-9697
DOI	10.1016/j.scitotenv.2024.172653
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Zs.A 949: Show issues

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Article: Spermidine inhibits LPS-induced pro-inflammatory activation of macrophages by acting on Nrf2 signaling but not autophagy

Guo, Fang-Fang / Meng, Fan-Ge / Zhang, Xiu-Ning / Zeng, Tao

Journal of functional foods. 2022 July, v. 94

2022

Abstract: This study was designed to investigate the roles of spermidine on lipopolysaccharide (LPS)-induced macrophage activation and underlying mechanisms. Spermidine was found to induce a moderate activation of autophagy but robust activation of nuclear factor ... ...

Abstract	This study was designed to investigate the roles of spermidine on lipopolysaccharide (LPS)-induced macrophage activation and underlying mechanisms. Spermidine was found to induce a moderate activation of autophagy but robust activation of nuclear factor erythroid 2-related factor 2 (Nrf-2) in a murine macrophage cell line RAW264.7 cells. Spermidine blunted LPS-driven proinflammatory activation of RAW264.7 cells evidenced by the reduced release of NO, TNF-α, and reactive oxygen species (ROS). The effects of spermidine were not affected by the autophagy inhibitor, while the autophagy inducers could not block the activation of macrophages induced by LPS. Interestingly, Nrf-2 inducers significantly suppressed the secretion of NO and TNF-α in RAW264.7 cells exposed to LPS, while the roles of spermidine were significantly blunted by the knockout of Nrf-2. Furthermore, spermidine suppressed the activation of NF-κB and the NLRP3 inflammasome in mouse liver. Collectively, spermidine could suppress LPS-induced macrophages activation possibly by activating Nrf-2 in macrophages.
Keywords	autophagy ; cell lines ; inflammasomes ; lipopolysaccharides ; liver ; macrophage activation ; macrophages ; mice ; reactive oxygen species ; secretion ; spermidine
Language	English
Dates of publication	2022-07
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2511964-3
ISSN	1756-4646
ISSN	1756-4646
DOI	10.1016/j.jff.2022.105115
Database	NAL-Catalogue (AGRICOLA)

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Z 7830: Show issues

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Article ; Online: Targeting macrophage polarization by Nrf2 agonists for treating various xenobiotics-induced toxic responses.

Wang, Yi-Ran / Zhang, Xiu-Ning / Meng, Fan-Ge / Zeng, Tao

Toxicology mechanisms and methods

2021 Volume 31, Issue 5, Page(s) 334–342

Abstract: Macrophages can polarize into different phenotypes in response to different microenvironmental stimuli. Macrophage polarization has been assigned to two extreme states, namely proinflammatory M1 and anti-inflammatory M2. Accumulating evidences have ... ...

Abstract	Macrophages can polarize into different phenotypes in response to different microenvironmental stimuli. Macrophage polarization has been assigned to two extreme states, namely proinflammatory M1 and anti-inflammatory M2. Accumulating evidences have demonstrated that M1 polarized macrophages contribute to various toxicants-induced deleterious effects. Switching macrophages from proinflammatory M1 phenotype toward anti-inflammatory M2 phenotype could be a promising approach for treating various inflammatory diseases. Studies in the past few decades have revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) can modulate the polarization of macrophages. Specifically, activation of Nrf2 could block M1 stimuli-induced production of proinflammatory cytokines and chemokines, and shift the polarization of macrophages toward M2 by cross-talking with nuclear factor kappa-B (NF-κB), mitogen-activated protein kinases (MAPKs), peroxisome proliferator-activated receptor γ (PPARγ), and autophagy. Importantly, a great number of studies have confirmed the beneficial effects of natural and synthesized Nrf2 agonists on various inflammatory diseases; however, most of these compounds are far away from clinical application due to lack of characterization and defects of study designs. Interestingly, some endogenous Nrf2 inducers and compounds with dual activities (such as the Nrf2 inducing and CO releasing effects) exhibit potent anti-inflammatory effects, which points out an important direction for future researches.
MeSH term(s)	Cytokines ; Macrophages ; NF-E2-Related Factor 2 ; NF-kappa B ; Xenobiotics/toxicity
Chemical Substances	Cytokines ; NF-E2-Related Factor 2 ; NF-kappa B ; Xenobiotics
Language	English
Publishing date	2021-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2081252-8
ISSN	1537-6524 ; 1537-6516 ; 1051-7235
ISSN (online)	1537-6524
ISSN	1537-6516 ; 1051-7235
DOI	10.1080/15376516.2021.1894624
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Zs.A 3215: Show issues

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Article: Diallyl disulfide suppresses the lipopolysaccharide-driven inflammatory response of macrophages by activating the Nrf2 pathway

Zhang, Xiu-Ning / Zhao, Ning / Guo, Fang-Fang / Wang, Yi-Ran / Liu, Shi-Xuan / Zeng, Tao

Food and chemical toxicology. 2022 Jan., v. 159

2022

Abstract: Lipopolysaccharide (LPS)-driven activation of Kupffer cells plays critical roles in the development of alcoholic liver disease (ALD). Accumulating evidence has revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) can modulate the polarization ...

Abstract	Lipopolysaccharide (LPS)-driven activation of Kupffer cells plays critical roles in the development of alcoholic liver disease (ALD). Accumulating evidence has revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) can modulate the polarization of macrophages. The current study aimed to investigate the roles of diallyl disulfide (DADS) in LPS-driven inflammation in vitro and in vivo. We found that DADS significantly increased the nuclear translocation of Nrf2 and the transcription of Nrf2 targets, including HO1, NQO1, and γ-GCSc, and suppressed degradation of Nrf2 protein. Besides, DADS significantly inhibited LPS-induced activation of NF-κB and MAPK, secretion of NO and TNF-α, and production of reactive oxygen species (ROS) in LPS-exposed RAW264.7 cells. In vivo study demonstrated that DADS significantly ameliorated liver damage in mice challenged with LPS, as shown by the inhibition of increases in serum aminotransferase activities, neutrophil infiltration, and NF-κB and NLRP3 inflammasome activation. Finally, knockout of Nrf2 abrogated the suppression of DADS on macrophage polarization and on liver injury induced by LPS. These findings reveal that DADS suppresses LPS-driven inflammatory response in the liver by activating Nrf2, which suggests that the protective effects of DADS against ALD may be attributed to the modulation of Kupffer cell polarization in the liver.
Keywords	blood serum ; diallyl disulfide ; inflammasomes ; inflammation ; lipopolysaccharides ; liver ; liver diseases ; neutrophils ; reactive oxygen species ; secretion ; toxicology
Language	English
Dates of publication	2022-01
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2021.112760
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Z 4035: Show issues

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Article ; Online: Diallyl disulfide suppresses the lipopolysaccharide-driven inflammatory response of macrophages by activating the Nrf2 pathway.

Zhang, Xiu-Ning / Zhao, Ning / Guo, Fang-Fang / Wang, Yi-Ran / Liu, Shi-Xuan / Zeng, Tao

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2021 Volume 159, Page(s) 112760

Abstract	Lipopolysaccharide (LPS)-driven activation of Kupffer cells plays critical roles in the development of alcoholic liver disease (ALD). Accumulating evidence has revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) can modulate the polarization of macrophages. The current study aimed to investigate the roles of diallyl disulfide (DADS) in LPS-driven inflammation in vitro and in vivo. We found that DADS significantly increased the nuclear translocation of Nrf2 and the transcription of Nrf2 targets, including HO1, NQO1, and γ-GCSc, and suppressed degradation of Nrf2 protein. Besides, DADS significantly inhibited LPS-induced activation of NF-κB and MAPK, secretion of NO and TNF-α, and production of reactive oxygen species (ROS) in LPS-exposed RAW264.7 cells. In vivo study demonstrated that DADS significantly ameliorated liver damage in mice challenged with LPS, as shown by the inhibition of increases in serum aminotransferase activities, neutrophil infiltration, and NF-κB and NLRP3 inflammasome activation. Finally, knockout of Nrf2 abrogated the suppression of DADS on macrophage polarization and on liver injury induced by LPS. These findings reveal that DADS suppresses LPS-driven inflammatory response in the liver by activating Nrf2, which suggests that the protective effects of DADS against ALD may be attributed to the modulation of Kupffer cell polarization in the liver.
MeSH term(s)	Allyl Compounds/pharmacology ; Animals ; Cell Polarity/drug effects ; Disulfides/pharmacology ; Kupffer Cells/drug effects ; Lipopolysaccharides/toxicity ; Liver/cytology ; Liver/drug effects ; Macrophages/drug effects ; Macrophages/immunology ; Mice ; NF-E2-Related Factor 2/metabolism ; RAW 264.7 Cells ; Signal Transduction/drug effects ; Signal Transduction/immunology
Chemical Substances	Allyl Compounds ; Disulfides ; Lipopolysaccharides ; NF-E2-Related Factor 2 ; diallyl disulfide (5HI47O6OA7)
Language	English
Publishing date	2021-12-09
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2021.112760
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Zs.A 529: Show issues

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Article ; Online: N,N-dimethylformamide-induced acute liver damage is driven by the activation of NLRP3 inflammasome in liver macrophages of mice.

Liu, Hong / Li, Ming-Jun / Zhang, Xiu-Ning / Wang, Shuo / Li, Long-Xia / Guo, Fang-Fang / Zeng, Tao

Ecotoxicology and environmental safety

2022 Volume 238, Page(s) 113609

Abstract: N,N-dimethylformamide (DMF) is a non-negligible volatile hazardous material in indoor and outdoor environments. Although the hepatotoxicity of DMF has been well recognized, the underlying mechanisms remain unclear and prophylactic medicine is still ... ...

Abstract	N,N-dimethylformamide (DMF) is a non-negligible volatile hazardous material in indoor and outdoor environments. Although the hepatotoxicity of DMF has been well recognized, the underlying mechanisms remain unclear and prophylactic medicine is still lacking. Herein, we established a DMF-induced acute liver injury mouse model and investigated the underlying mechanisms focusing on oxidative stress and the nucleotide-binding domain and leucine-rich repeat receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome. DMF was found to induce oxidative stress, evidenced by the elevation of hepatic malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) adducts levels, and the decline of reduced glutathione (GSH) levels. However, neither N-acetyl cysteine (NAC) nor sulforaphane (SF) ameliorated the hepatoxicity induced by DMF in mice. Interestingly, DMF exposure led to focal necrosis of hepatocytes and NLRP3 inflammasome activation before the onset of obvious liver damage. In addition, DMF exposure induced infiltration and proinflammatory/M1 polarization of macrophages in mice livers. Furthermore, the inactivation of hepatic macrophages by GdCl
MeSH term(s)	Animals ; Chemical and Drug Induced Liver Injury/etiology ; Dimethylformamide ; Inflammasomes ; Liver ; Liver Diseases ; Macrophages ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Dimethylformamide (8696NH0Y2X)
Language	English
Publishing date	2022-05-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2022.113609
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Zs.A 1418: Show issues

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Article ; Online: Transformed ALDH2

Zhang, Xiu-Ning / Meng, Fan-Ge / Wang, Yi-Ran / Liu, Shi-Xuan / Zeng, Tao

Medical hypotheses

2020 Volume 146, Page(s) 110366

Abstract: Alcohol is a well-recognized hepatic carcinogen. Alcohol is metabolized into genotoxic acetaldehyde in hepatocytes, which is catalyzed by aldehyde dehydrogenase 2 (ALDH2). The detailed underlying mechanisms of alcohol-related hepatocellular carcinoma ( ... ...

Abstract	Alcohol is a well-recognized hepatic carcinogen. Alcohol is metabolized into genotoxic acetaldehyde in hepatocytes, which is catalyzed by aldehyde dehydrogenase 2 (ALDH2). The detailed underlying mechanisms of alcohol-related hepatocellular carcinoma (HCC) remains unclear, at least partially, due to the absence of appropriate experimental models. Current studies suggest that rodents are not good models of the most common liver diseases that trigger HCC including alcoholic liver injury. We hypothesize that ethanol could induce transformation of immortalized normal liver cells, which may serve as a versatile tool for studying alcoholic HCC. Besides, we believe that knockout of ALDH2 will help to shorten the time course of transformation, as ALDH2 deficiency will significantly increase the accumulation of acetaldehyde in hepatocytes. Using this model, the dynamic changes of carcinogenesis-related molecular events could be easily examined. Furthermore, the transformed cells isolated from soft agar could be inoculated to mice for studying invasion, metastasis, and also for screening prophylactics.
MeSH term(s)	Acetaldehyde/toxicity ; Aldehyde Dehydrogenase ; Aldehyde Dehydrogenase, Mitochondrial ; Animals ; Carcinogenesis ; Carcinoma, Hepatocellular ; Ethanol/toxicity ; Hepatocytes ; Liver Neoplasms ; Mice
Chemical Substances	Ethanol (3K9958V90M) ; ALDH2 protein, mouse (EC 1.2.1.3) ; Aldehyde Dehydrogenase (EC 1.2.1.3) ; Aldehyde Dehydrogenase, Mitochondrial (EC 1.2.1.3) ; Acetaldehyde (GO1N1ZPR3B)
Language	English
Publishing date	2020-11-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	193145-3
ISSN	1532-2777 ; 0306-9877
ISSN (online)	1532-2777
ISSN	0306-9877
DOI	10.1016/j.mehy.2020.110366
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Article ; Online: Roles of peroxisome proliferator-activated receptor α in the pathogenesis of ethanol-induced liver disease.

Meng, Fan-Ge / Zhang, Xiu-Ning / Liu, Shi-Xuan / Wang, Yi-Ran / Zeng, Tao

Chemico-biological interactions

2020 Volume 327, Page(s) 109176

Abstract: Alcoholic liver disease (ALD) is a progressively aggravated liver disease with high incidence in alcoholics. Ethanol-induced fat accumulation and the subsequent lipopolysaccharide (LPS)-driven inflammation bring liver from reversible steatosis, to ... ...

Abstract	Alcoholic liver disease (ALD) is a progressively aggravated liver disease with high incidence in alcoholics. Ethanol-induced fat accumulation and the subsequent lipopolysaccharide (LPS)-driven inflammation bring liver from reversible steatosis, to irreversible hepatitis, fibrosis, cirrhosis, and even hepatocellular carcinoma. Peroxisome proliferator-activated receptor α (PPARα) is a member of the nuclear receptor superfamily of ligand-activated transcription factors and plays pivotal roles in the regulation of fatty acid homeostasis as well as the inflammation control in the liver. It has been well documented that PPARα activity and/or expression are downregulated in liver of mice exposed to ethanol, which is thought to be one of the prime contributors to ethanol-induced steatosis, hepatitis and fibrosis. This article summarizes the current evidences from in vitro and animal models for the critical roles of PPARα in the onset and progression of ALD. Importantly, it should be noted that the expression of PPARα in human liver is reported to be similar to that in mice, and PPARα expression is downregulated in the liver of patients with nonalcoholic fatty liver disease (NAFLD), a disease sharing many similarities with ALD. Therefore, clinical trials investigating the expression of PPARα in the liver of ALD patients and the efficacy of strong PPARα agonists for the prevention and treatment of ALD are warranted.
MeSH term(s)	Adiponectin/metabolism ; Animals ; Circadian Rhythm Signaling Peptides and Proteins/metabolism ; Down-Regulation ; Ethanol ; Fatty Liver, Alcoholic/etiology ; Fatty Liver, Alcoholic/metabolism ; Humans ; Inflammation/chemically induced ; Inflammation/etiology ; Inflammation/metabolism ; Liver/metabolism ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/etiology ; Liver Cirrhosis/metabolism ; Liver Neoplasms/chemically induced ; Liver Neoplasms/etiology ; Liver Neoplasms/metabolism ; PPAR alpha/agonists ; PPAR alpha/metabolism ; Sterol Regulatory Element Binding Protein 1/metabolism
Chemical Substances	Adiponectin ; Circadian Rhythm Signaling Peptides and Proteins ; PPAR alpha ; Sterol Regulatory Element Binding Protein 1 ; Ethanol (3K9958V90M)
Language	English
Publishing date	2020-06-11
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2020.109176
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Article ; Online: Allyl methyl disulfide (AMDS) prevents N,N-dimethyl formamide-induced liver damage by suppressing oxidative stress and NLRP3 inflammasome activation.

Li, Long-Xia / Wang, Lin / Wang, Shuo / Zhang, Xiu-Ning / Liu, Hong / Zhang, Yan-Jing / Wu, Chuan-Tao / Zhang, Cui-Li / Zeng, Tao

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2023 Volume 182, Page(s) 114198

Abstract: N,N-dimethylformamide (DMF), a widely consumed industrial solvent with persistent characteristics, can induce occupational liver damage and pose threats to the general population due to the enormous DMF-containing industrial efflux and emission from ... ...

Abstract	N,N-dimethylformamide (DMF), a widely consumed industrial solvent with persistent characteristics, can induce occupational liver damage and pose threats to the general population due to the enormous DMF-containing industrial efflux and emission from indoor facilities. This study was performed to explore the roles of allyl methyl disulfide (AMDS) in liver damage induced by DMF and the underlying mechanisms. AMDS was found to effectively suppress the elevation in the liver weight/body weight ratio and serum aminotransferase activities, and reduce the mortality of mice induced by DMF. In addition, AMDS abrogated DMF-elicited increases in malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels and decreases in glutathione (GSH) levels in mouse livers. The increase in macrophage number, mRNA expression of M1 macrophage biomarkers, and protein expression of key components in the NF-κB pathway and NLRP3 inflammasome induced by DMF exposure were all suppressed by AMDS in mouse livers. Furthermore, AMDS inhibited DMF-induced cell damage and NF-κB activation in cocultured AML12 hepatocytes and J774A.1 macrophages. However, AMDS per se did not significantly affect the protein level and activity of CYP2E1. Collectively, these results demonstrate that AMDS effectively ameliorates DMF-induced acute liver damage possibly by suppressing oxidative stress and inactivating the NF-κB pathway and NLRP3 inflammasome.
MeSH term(s)	Humans ; Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NF-kappa B/metabolism ; Dimethylformamide/toxicity ; Dimethylformamide/metabolism ; Liver Diseases/metabolism ; Oxidative Stress ; Liver ; Glutathione/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NF-kappa B ; allyl methyl disulfide (OXW45UTR7B) ; Dimethylformamide (8696NH0Y2X) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2023-11-21
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2023.114198
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