ArticleFrontiers in physiology2012
Glutathione supplementation attenuates lipopolysaccharide-induced mitochondrial dysfunction and apoptosis in a mouse model of acute lung injury.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Development and validation of a bedside prognostic model for in-hospital mortality in acute diquat poisoning.BMC emergency medicine · 2026Article
- Glabridin attenuates LTA‑induced alveolar macrophage migration via activation of the Nrf2/HO‑1 pathway.Molecular medicine reports · 2026Article
- The Impact of LPS on Inflammatory Responses in Alpha-Tocopherol Deficient Mice.Current developments in nutrition · 2024Article
- Reactive Oxygen Species and Strategies for Antioxidant Intervention in Acute Respiratory Distress Syndrome.Antioxidants (Basel, Switzerland) · 2023Review
- L-citrulline attenuates lipopolysaccharide-induced inflammatory lung injury in neonatal rats.Pediatric research · 2023Article
- Ferroptosis, pyroptosis and necroptosis in acute respiratory distress syndrome.Cell death discovery · 2023Review
- TLR4 activation induces inflammatory vascular permeability via Dock1 targeting and NOX4 upregulation.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Polyphenols-Rich Fraction fromPharmaceutics · 2022Article
- The role of oxidative stress in the pathogenesis of infections with coronaviruses.Frontiers in microbiology · 2022Review
- Glutathione ethyl ester reverses the deleterious effects of fentanyl on ventilation and arterial blood-gas chemistry while prolonging fentanyl-induced analgesia.Scientific reports · 2021Article
- Mechanisms Underlying the Effects of Lianhua Qingwen on Sepsis-Induced Acute Lung Injury: A Network Pharmacology Approach.Frontiers in pharmacology · 2021Article
- The Role of Ferroptosis in Acute Respiratory Distress Syndrome.Frontiers in medicine · 2021Review
- Novel Antioxidant Therapy with the Immediate Precursor to Glutathione, γ-Glutamylcysteine (GGC), Ameliorates LPS-Induced Cellular Stress in In Vitro 3D-Differentiated Airway Model from Primary Cystic Fibrosis Human Bronchial Cells.Antioxidants (Basel, Switzerland) · 2020Article
- Regulatory mechanism of NOV/CCN3 in the inflammation and apoptosis of lung epithelial alveolar cells upon lipopolysaccharide stimulation.Molecular medicine reports · 2020Article
- TIPE2 ameliorates lipopolysaccharide-induced apoptosis and inflammation in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- ASK1-p38 cascaded signal mediates pulmonary microvascular endothelial barrier injury induced by the return of PHSML in rats.RSC advances · 2019Article
- GSH-C4 Acts as Anti-inflammatory Drug in Different Models of Canonical and Cell Autonomous Inflammation Through NFκB Inhibition.Frontiers in immunology · 2019Article
- Inhibition of interleukin-6 trans-signaling prevents inflammation and endothelial barrier disruption in retinal endothelial cells.Experimental eye research · 2019Article
- Endothelial cell signaling and ventilator-induced lung injury: molecular mechanisms, genomic analyses, and therapeutic targets.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Perioperative "remote" acute lung injury: recent update.Journal of biomedical research · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury (ALI) is a life threatening condition associated with hypoxemia, diffuse alveolar damage, inflammation, and loss of lung function. Lipopolysaccharide (LPS; endotoxin) from the outer membrane of Gram-negative bacteria is a major virulence factor involved in the development of ALI. The depletion of glutathione (GSH), an essential intra- and extra-cellular protective antioxidant, by LPS is an important event that contributes to the elevation in reactive oxygen species. Whether restoring GSH homeostasis can effectively ameliorate mitochondrial dysfunction and cellular apoptosis in ALI is unknown and therefore, was the focus of this study. In peripheral lung tissue of LPS-treated mice, hydrogen peroxide and protein nitration levels were significantly increased. Pre-treatment with GSH-ethyl ester (GSH-EE) prevented this increase in oxidative stress. LPS also increased the lactate/pyruvate ratio, attenuated SOD2 protein levels, and decreased ATP levels in the mouse lung indicative of mitochondrial dysfunction. Again, GSH-EE treatment preserved the mitochondrial function. Finally, our studies showed that LPS induced an increase in the mitochondrial translocation of Bax, caspase 3 activation, and nuclear DNA fragmentation and these parameters were all prevented with GSH-EE. Thus, this study suggests that GSH-EE supplementation may reduce the mitochondrial dysfunction associated with ALI.
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