Study on the potential way of hepatic cytotoxicity of <i>N</i>,<i>N</i>‐dimethylformamide

Li, Shiqing; Wang, Cui

doi:10.1002/jbt.22190

Cited by 14 publications

(5 citation statements)

References 31 publications

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“…Similarly, the Group 1 carcinogen trichloroethylene (79-01-6) enriched Prostate Cancer, Hepatocellular Carcinoma, and four similar pathways, which is consistent with epidemiological studies that linked this chemical to liver and prostate cancer in humans with significant exposures . The Group 2A carcinogen dimethylformamide (68-12-2) induces apoptosis in liver cells through the p53 pathway and maintains a redox status imbalance . Consistent with these findings, dimethylformamide enriched 13 apoptosis-related pathways (e.g., Apoptosis), 16 TP53/p53-related pathways (e.g., p53 Pathway), and oxidative stress pathways (e.g., Oxidative Stress Induced Senescence).…”

Section: Discussionsupporting

confidence: 77%

“… 58 The Group 2A carcinogen dimethylformamide (68-12-2) induces apoptosis in liver cells through the p53 pathway and maintains a redox status imbalance. 59 Consistent with these findings, dimethylformamide enriched 13 apoptosis-related pathways (e.g., Apoptosis), 16 TP53/p53-related pathways (e.g., p53 Pathway), and oxidative stress pathways (e.g., Oxidative Stress Induced Senescence).…”

Section: Discussionsupporting

confidence: 56%

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The Known and Unknown: Investigating the Carcinogenic Potential of Plastic Additives

Vincoff,

Schleupner,

Santos

et al. 2024

Environ. Sci. Technol.

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Microplastics are routinely ingested and inhaled by humans and other organisms. Despite the frequency of plastic exposure, little is known about its health consequences. Of particular concern are plastic additives�chemical compounds that are intentionally or unintentionally added to plastics to improve functionality or as residual components of plastic production. Additives are often loosely bound to the plastic polymer and may be released during plastic exposures. To better understand the health effects of plastic additives, we performed a comprehensive literature search to compile a list of 2,712 known plastic additives. Then, we performed an integrated toxicogenomic analysis of these additives, utilizing cancer classifications and carcinogenic expression pathways as a primary focus. Screening these substances across two chemical databases revealed two key observations: (1) over 150 plastic additives have known carcinogenicity and (2) the majority (∼90%) of plastic additives lack data on carcinogenic end points. Analyses of additive usage patterns pinpointed specific polymers, functions, and products in which carcinogenic additives reside. Based on published chemical−gene interactions, both carcinogenic additives and additives with unknown carcinogenicity impacted similar biological pathways. The predominant pathways involved DNA damage, apoptosis, the immune response, viral diseases, and cancer. This study underscores the urgent need for a systematic and comprehensive carcinogenicity assessment of plastic additives and regulatory responses to mitigate the potential health risks of plastic exposure.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 56%

The Known and Unknown: Investigating the Carcinogenic Potential of Plastic Additives

Vincoff,

Schleupner,

Santos

et al. 2024

Environ. Sci. Technol.

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“…Changes in MMP were measured using the MMP assay kit with JC-1(Beyotime Biotechnology, Shanghai, China) as described previously [19].…”

Section: Measurement Of Mitochondrial Membrane Potential (Mmp)mentioning

confidence: 99%

CLIC1 Inhibition Protects Against Cellular Senescence and Endothelial Dysfunction Via the Nrf2/HO-1 Pathway

Ding

et al. 2021

Cell Biochem Biophys

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Chloride intracellular channel 1 (CLIC1) is a sensor of oxidative stress in endothelial cells (EC). However, the mechanism by which CLIC1 mediate the regulation of endothelial dysfunction has not been established. In this study, overexpressed CLIC1 impaired the ability of the vascular cells to resist oxidative damage and promoted cellular senescence. Besides, suppressed CLIC1 protected against cellular senescence and dysfunction in Human Umbilical Vein Endothelial Cells (HUVECs) through the Nrf2/HO-1 pathway. We also found that ROS-activated CLIC1-induced oxidative stress in HUVECs. Nrf2 nuclear translocation was inhibited by CLIC1 overexpression, but was enhanced by IAA94 (CLICs inhibitor) treatment or knockdown of CLIC1. The Nrf2/HO-1 pathway plays a critical role in the anti-oxidative effect of suppressing CLIC1. And inhibition of CLIC1 decreases oxidative stress injury by downregulating the levels of ROS, MDA, and the expression of EC effectors (ICAM1 and VCAM1) protein expression and promotes the activity of superoxide dismutase (SOD). The AMPK-mediated signaling pathway activates Nrf2 through Nrf2 phosphorylation and nuclear translocation, which is also regulated by CLIC1. Moreover, the activation of CLIC1 contributes to H 2 O 2-induced mitochondrial dysfunction and activation of mitochondrial fission. Therefore, elucidation of the mechanisms by which CLIC1 is involved in these pivotal pathways may uncover its therapeutic potential in alleviating ECs oxidative stress and age-related cardiovascular disease development.

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“…Previous studies have indicated that overdose of DMF causes hepatic cytotoxicity, 39 , 40 which leads to the consideration of choosing the appropriate dose for disease treatment. Moreover, DMF is known to elicit certain alcohol intolerance reactions.…”

Section: Discussionmentioning

confidence: 99%

N,N-Dimethylformamide inhibits high glucose-induced osteoporosis via attenuating MAPK and NF-κB signalling

Liu

2022

Bone & Joint Research

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Aims The role of N,N-dimethylformamide (DMF) in diabetes-induced osteoporosis (DM-OS) progression remains unclear. Here, we aimed to explore the effect of DMF on DM-OS development. Methods Diabetic models of mice, RAW 264.7 cells, and bone marrow macrophages (BMMs) were established by streptozotocin stimulation, high glucose treatment, and receptor activator of nuclear factor-κB ligand (RANKL) treatment, respectively. The effects of DMF on DM-OS development in these models were examined by micro-CT analysis, haematoxylin and eosin (H&E) staining, osteoclast differentiation of RAW 264.7 cells and BMMs, H&E and tartrate-resistant acid phosphatase (TRAP) staining, enzyme-linked immunosorbent assay (ELISA) of TRAP5b and c-terminal telopeptides of type 1 (CTX1) analyses, reactive oxygen species (ROS) analysis, quantitative reverse transcription polymerase chain reaction (qRT-PCR), Cell Counting Kit-8 (CCK-8) assay, and Western blot. Results The established diabetic mice were more sensitive to ovariectomy (OVX)-induced osteoporosis, and DMF treatment inhibited the sensitivity. OVX-treated diabetic mice exhibited higher TRAP5b and c-terminal telopeptides of type 1 (CTX1) levels, and DMF treatment inhibited the enhancement. DMF reduced RAW 264.7 cell viability. Glucose treatment enhanced the levels of TRAP5b, cathepsin K, Atp6v0d2, and H+-ATPase, ROS, while DMF reversed this phenotype. The glucose-increased protein levels were inhibited by DMF in cells treated with RANKL. The expression levels of antioxidant enzymes Gclc, Gclm, Ho-1, and Nqo1 were upregulated by DMF. DMF attenuated high glucose-caused osteoclast differentiation by targeting mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signalling in BMMs. Conclusion DMF inhibits high glucose-induced osteoporosis by targeting MAPK and NF-κB signalling. Cite this article: Bone Joint Res 2022;11(4):200–209.

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Study on the potential way of hepatic cytotoxicity of N,N‐dimethylformamide

Cited by 14 publications

References 31 publications

The Known and Unknown: Investigating the Carcinogenic Potential of Plastic Additives

The Known and Unknown: Investigating the Carcinogenic Potential of Plastic Additives

CLIC1 Inhibition Protects Against Cellular Senescence and Endothelial Dysfunction Via the Nrf2/HO-1 Pathway

N,N-Dimethylformamide inhibits high glucose-induced osteoporosis via attenuating MAPK and NF-κB signalling

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