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Background: Phosgene is a chemical material widely used worldwide. No effective method has been developed to reverse its pathological injuries. Some studies have shown that neuronal inflammation in lung tissue is involved, but the specific mechanism has not been reported.

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Alpha-1 antitrypsin protects against phosgene-induced acute lung injury by activating the ID1-dependent anti-inflammatory response.

Eur J Pharmacol

October 2023

Department of Toxicology, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032, China. Electronic address:

Article Synopsis
  • * Alpha-1 antitrypsin (α1-AT), a protease inhibitor used for emphysema, has been shown to have anti-inflammatory properties and may help treat phosgene-induced ALI.
  • * The study found that α1-AT is produced by neutrophils in response to phosgene exposure and that administering α1-AT can reduce inflammation and cell death by activating a protective mechanism involving the ID1 gene.
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Purpose: Chemically induced acute lung injury (CALI) has become a serious health concern in our industrialized world, and abnormal functional alterations of immune cells crucially contribute to severe clinical symptoms. However, the cell heterogeneity and functional phenotypes of respiratory immune characteristics related to CALI remain unclear.

Methods: We performed scRNA sequencing on bronchoalveolar lavage fluid (BALF) samples obtained from phosgene-induced CALI rat models and healthy controls.

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PTTG1 promotes CD34CD45 cells to repair the pulmonary vascular barrier via activating the VEGF-bFGF/PI3K/AKT/eNOS signaling pathway in rats with phosgene-induced acute lung injury.

Biomed Pharmacother

June 2023

Center of Emergency and Critical Medicine, Jinshan Hospital of Fudan University, China; Research Center for Chemical Injury, Emergency and Critical Medicine of Fudan University, China; Key Laboratory of Chemical Injury, Emergency and Critical Medicine of Shanghai Municipal Health Commission, China. Electronic address:

Accidental exposure to phosgene can cause acute lung injury (ALI), characterized by uncontrolled inflammation and impaired lung blood-gas barrier. CD34CD45 cells with high pituitary tumor transforming gene 1 (PTTG1) expression were identified around rat pulmonary vessels through single-cell RNA sequencing, and have been shown to attenuate P-ALI by promoting lung vascular barrier repair. As a transcription factor closely related to angiogenesis, whether PTTG1 plays a role in CD34CD45 cell repairing the pulmonary vascular barrier in rats with P-ALI remains unclear.

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Article Synopsis
  • - Carbon tetrachloride (CCl) is a toxic compound that causes liver damage in animal studies by being processed in the body, leading to harmful byproducts like phosgene.
  • - The study discovered a modification in the liver protein D-dopachrome tautomerase (DDT) after exposure to CCl, specifically a glutathionyl carbonylated group formed from phosgene and reduced glutathione (GSH).
  • - Furthermore, researchers found that macrophage migration inhibitory factor (MIF), which shares similarities with DDT, also had a glutathionyl-carbonylated modification, suggesting that proteins in the MIF family are particularly affected by this process.
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