scholarly journals Octacosanol Attenuates Disrupted Hepatic Reactive Oxygen Species Metabolism Associated with Acute Liver Injury Progression in Rats Intoxicated with Carbon Tetrachloride

2008 ◽  
Vol 42 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Yoshiji Ohta ◽  
Koji Ohashi ◽  
Tatsuya Matsura ◽  
Kenji Tokunaga ◽  
Akira Kitagawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Injury Progression ◽  
Reactive Oxygen Species Metabolism

scholarly journals Melatonin prevents disruption of hepatic reactive oxygen species metabolism in rats treated with carbon tetrachloride

2004 ◽  
Vol 36 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Yoshiji Ohta ◽  
Mutsumi Kongo-Nishimura ◽  
Tatsuya Matsura ◽  
Kazuo Yamada ◽  
Akira Kitagawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Carbon Tetrachloride ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Reactive Oxygen Species Metabolism

Reactive oxygen species-responsive polymeric nanoparticles for alleviating sepsis-induced acute liver injury in mice

Biomaterials ◽  
2017 ◽  
Vol 144 ◽  
pp. 30-41 ◽  
Author(s):  
Gan Chen ◽  
Hongzhang Deng ◽  
Xiang Song ◽  
Mingzi Lu ◽  
Lian Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Polymeric Nanoparticles ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1243
Author(s):  
Eunus S. Ali ◽  
Grigori Y. Rychkov ◽  
Greg J. Barritt
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Chronic Liver ◽  
Oxygen Species ◽  
Alcoholic Fatty Liver ◽  
Trpm2 Channels

TRPM2 channels admit Ca2+ and Na+ across the plasma membrane and release Ca2+ and Zn2+ from lysosomes. Channel activation is initiated by reactive oxygen species (ROS), leading to a subsequent increase in ADP-ribose and the binding of ADP-ribose to an allosteric site in the cytosolic NUDT9 homology domain. In many animal cell types, Ca2+ entry via TRPM2 channels mediates ROS-initiated cell injury and death. The aim of this review is to summarise the current knowledge of the roles of TRPM2 and Ca2+ in the initiation and progression of chronic liver diseases and acute liver injury. Studies to date provide evidence that TRPM2-mediated Ca2+ entry contributes to drug-induced liver toxicity, ischemia–reperfusion injury, and the progression of non-alcoholic fatty liver disease to cirrhosis, fibrosis, and hepatocellular carcinoma. Of particular current interest are the steps involved in the activation of TRPM2 in hepatocytes following an increase in ROS, the downstream pathways activated by the resultant increase in intracellular Ca2+, and the chronology of these events. An apparent contradiction exists between these roles of TRPM2 and the role identified for ROS-activated TRPM2 in heart muscle and in some other cell types in promoting Ca2+-activated mitochondrial ATP synthesis and cell survival. Inhibition of TRPM2 by curcumin and other “natural” compounds offers an attractive strategy for inhibiting ROS-induced liver cell injury. In conclusion, while it has been established that ROS-initiated activation of TRPM2 contributes to both acute and chronic liver injury, considerable further research is needed to elucidate the mechanisms involved, and the conditions under which pharmacological inhibition of TRPM2 can be an effective clinical strategy to reduce ROS-initiated liver injury.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

Extract of Dorema aucheri induces PPAR-γ for activating reactive oxygen species metabolism

2016 ◽  
Vol 6 (4) ◽  
pp. 171-179 ◽  
Author(s):  
Mohammadreza Nahvinejad ◽  
Fatemeh Pourrajab ◽  
Seyedhossein Hekmatimoghaddam
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ppar Γ ◽  
Reactive Oxygen Species Metabolism
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