Performance of extracorporeal membrane oxygenation in patients with fatal paraquat poisoning: grasp for straws?

Feng, Meng-Xiao; Lu, Yuan-Qiang

doi:10.5847/wjem.j.1920-8642.2021.03.013

Cited by 2 publications

(2 citation statements)

References 9 publications

(15 reference statements)

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“…If the preceding efforts failed, we used V-A ECMO to maintain the patient's circulation and oxygenation. 9 …”

Section: Methodsmentioning

confidence: 99%

“…PQ results in acute lung injury in the early stages and pulmonary fibrosis in the later stages. 9 , 10 Several case reports showed that acute high-dose DQ poisoning usually affected the kidneys, liver, brain, and heart. 11 , 12 , 13 , 14 Current toxicology studies indicate that DQ does not covalently bind to macromolecules (i.e., lipids, proteins and nucleic acids), but it can generate reactive oxygen species (ROS) in cells through an oxidation–reduction cycle process, resulting in increased phospholipid membrane permeability and subsequent cell membrane rupture.…”

Section: Introductionmentioning

confidence: 99%

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Lethal diquat poisoning manifests as acute central nervous system injury and circulatory failure: A retrospective cohort study of 50 cases

Zhou

Lu²

2022

eClinicalMedicine

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“…If the preceding efforts failed, we used V-A ECMO to maintain the patient's circulation and oxygenation. 9 …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lethal diquat poisoning manifests as acute central nervous system injury and circulatory failure: A retrospective cohort study of 50 cases

Zhou

Lu²

2022

eClinicalMedicine

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Mutual promotion of mitochondrial fission and oxidative stress contributes to mitochondrial-DNA-mediated inflammation and epithelial-mesenchymal transition in paraquat-induced pulmonary fibrosis

Zhang¹

2023

World J Emerg Med

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BACKGROUND: Pulmonary fibrosis (PF) is one of the main causes of death in patients with paraquat (PQ) poisoning. This study aimed to evaluate the relationship between mitochondrial fi ssion and oxidative stress in PQ-induced epithelial-mesenchymal transition (EMT) and PF.METHODS: C57BL/6 mice and MLE-12 cells were exposed to PQ to construct a PF model in vivo and in vitro. Histological changes in the lungs were examined by hematoxylin and eosin (H&E) staining. Mitochondrial morphology was detected by MitoTracker ® Deep Red FM or transmission electron microscopy (TEM). Western blotting and immunofluorescence were used to determine the expression of protein. The migration ability of the cells was detected by the cell scratch test. Mitochondrial DNA (mtDNA) levels were assessed by real-time polymerase chain reaction (PCR). Enzyme-linked immunosorbent assay (ELISA) was applied to detect cytokine levels. Superoxide dismutase (SOD) activity and the levels of glutathione (GSH) and malondialdehyde (MDA) were detected by chemichromatometry.RESULTS: PQ exposure caused EMT and PF in vivo and in vitro. PQ destroyed mitochondrial structure and enhanced the expression of dynamin-related protein 1 (Drp1), which were accompanied by oxidative stress. Inhibiting mitochondrial fission using mitochondrial division inhibitor-1 (Mdivi-1), a selective inhibitor of Drp1, attenuated PQ-induced EMT and oxidative damage. Treatment with N-acetyl-L-cysteine (NAC), an antioxidant, reduced Drp1 expression, attenuated mitochondrial structure damage and inhibited PQ-induced EMT and PF. Both Mdivi-1 and NAC treatment markedly suppressed mtDNA release, the expression of Toll-like receptor 9 (TLR9) and phosphorylation (P)-NF-κB p65 as well as cytokines (interleukin 6 [IL-6], interleukin-1β [IL-1β], and tumor necrosis factor-α [TNF-α]) production.CONCLUSION: Mutual promotion of mitochondrial fission and oxidative stress contributes to EMT in PQ-induced PF, which is associated with the mtDNA/TLR9/NF-κB pathway.

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Performance of extracorporeal membrane oxygenation in patients with fatal paraquat poisoning: grasp for straws?

Cited by 2 publications

References 9 publications

Lethal diquat poisoning manifests as acute central nervous system injury and circulatory failure: A retrospective cohort study of 50 cases

Lethal diquat poisoning manifests as acute central nervous system injury and circulatory failure: A retrospective cohort study of 50 cases

Mutual promotion of mitochondrial fission and oxidative stress contributes to mitochondrial-DNA-mediated inflammation and epithelial-mesenchymal transition in paraquat-induced pulmonary fibrosis

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