Original contributionLipid peroxidation as molecular mechanism of liver cell injury during reperfusion after ischemia
References (47)
Reactive oxygen and ischemia/reperfusion injury of the liver
Chem. Biol. Interact.
(1991)- et al.
Glutathione and ischemia-reperfusion injury in the perfused rat liver
Free Radic. Biol. Med.
(1992) - et al.
Inhibition of ischemia and reflow-induced liver injury by an SOD derivative that circulates bound to albumin
Arch. Biochem. Biophys.
(1990) - et al.
Mechanism and prevention of ischemia-reperfusion-induced liver injury in rats
J. Surg. Res.
(1991) - et al.
Breath ethane: A specific indicator of free-radical-mediated lipid peroxidation following reperfusion of the ischemic liver
Free Radic. Biol. Med.
(1992) - et al.
Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia
J. Surg. Res.
(1990) - et al.
Radiochemical quantitation of conjugated dienes during ischemia and reperfusion in the rat liver
Clin. Biochem.
(1991) - et al.
Chemiluminescence-HPLC assay of phosphatidylcholine hydroperoxide generated by ischemia-reperfusion in the liver of rats
Biochem. Pharmacol.
(1992) - et al.
Quantitation of lipid peroxidation products by gas chromatography-mass spectrometry
Anal. Biochem.
(1986) - et al.
The role of allyl alcohol-induced lipid peroxidation and liver cell damage in mice
Biochem. Pharmacol.
(1987)
NADH-dependent reductive stress and ferritin-bound iron in allyl alcohol-induced lipid peroxidation in vivo: The protective effect of vitamin E
Chem. Biol. Interact.
Drug-induced lipid peroxidation in mice II: Protection against paracetamol-induced liver necrosis by intravenous liposomally entrapped glutathione
Biochem. Pharmacol.
Noncyclooxygenase oxidative formation of a series of novel prostaglandins: Analytical ramification for measurement of eicosanoids
Anal. Biochem.
Quantitation of hydroperoxy-eicosatetraenoic acids and hydroxy-eicosatetraenoic acids as indicators of lipid peroxidation using gas chromatography-mass spectrometry
Anal. Biochem.
Role of leukotriene B4 in the pathogenesis of hepatic ischemia-reperfusion injury in the rat
Prostaglandins, Leukotr. Essent. Fatty Acids
tert-Butyl hydroperoxide kills cultured hepatocytes by peroxidizing membrane lipids
Arch. Biochem. Biophys.
Glutathione disulfide formation and lipid peroxidation during cardiac ischemia and reflow in the dog in vivo
Biochem. Biophys. Res. Commun.
Oxidation in the NADP system and release of GSSG from hemoglobin-free perfused rat liver during peroxidatic oxidation of glutathione by hydroperoxides
FEBS Lett.
Pathophysiological consequences of enhanced intracellular superoxide formation in isolated perfused rat liver
Chem. Biol. Interact.
Reactive oxygen species during ischemia-reflow injury in isolated perfused rat liver
J. Clin. Invest.
Oxidant stress during reperfusion of ischemic liver: No evidence for a role of xanthine oxidase
Hepatology
Cytochemical studies of hydrogen peroxide generation in postischemic hepatocytes
Am. J. Physiol.
Neutrophil and Kupffer cell-induced oxidant stress and ischemia-reperfusion injury in rat liver
Am. J. Physiol.
Cited by (165)
Recommendations for the use of the acetaminophen hepatotoxicity model for mechanistic studies and how to avoid common pitfalls
2021, Acta Pharmaceutica Sinica BCitation Excerpt :However, under normal circumstances when animals are fed a regular diet, ethane exhalation and other LPO markers such as MDA only increased 2–3-fold112–114 or did not increase at all115. When compared to the orders of magnitude increase observed in known models of lipid peroxidation-induced cell death115,116, these comparatively small increases in LPO markers suggest that LPO does not occur at a high enough level to directly cause cell death in APAP hepatotoxicity. When measuring LPO markers in APAP-induced liver injury, which includes mainly MDA and HNE, quantitative aspects need to be kept in mind.
Oxidative stress and acute hepatic injury
2018, Current Opinion in ToxicologyCitation Excerpt :Interestingly, lipid peroxidation was considered the main mechanism by which oxidant stress causes cell death during hepatic ischemia-reperfusion and other liver disease processes [46]. However, many lipid peroxidation parameters are elevated only 2-to-3-times above baseline despite severe liver reperfusion injury [47]. In contrast, it was shown that it requires a very severe oxidant stress by t-butyl hydroperoxide to cause sufficient lipid peroxidation (50-times above baseline) that can kill hepatocytes [47].
Reactive Oxygen and Nitrogen Species and Liver Ischemia-Reperfusion Injury: An Overview
2018, The Liver: Oxidative Stress and Dietary AntioxidantsUrinary F<inf>2</inf>-Isoprostane Concentration as a Poor Prognostic Factor After Subarachnoid Hemorrhage.
2017, World NeurosurgeryCitation Excerpt :For these reasons, urinary F2-IsoPs are among the most promising biomarkers of general oxidative stress. Elevated levels of urinary F2-IsoPs have been reported in numerous conditions, including alcoholic liver disease,33,34 hepatorenal syndrome,35 acute cholestasis,36,37 ischemia/reperfusion injury,38-41 diabetes,42,43 chronic obstructive pulmonary disease,44 allergic asthma,45 acute respiratory distress syndrome,46 Alzheimer disease,47-49 Huntington disease,50 retinopathy of prematurity,51,52 smoking,53,54 oxidative modification of low-density lipoprotein and atherogenesis,55-57 renal failure,58,59 and hyperhomocysteinemia.60 Therefore, we aimed to quantify urinary F2-IsoPs in patients with aSAH and to investigate their association with clinical aspects.
The relationship between plasma lipid peroxidation products and primary graft dysfunction after lung transplantation is modified by donor smoking and reperfusion hyperoxia
2016, Journal of Heart and Lung Transplantation