Role of lipid peroxidation in tissue injury after hepatic ischemia

Silver, E.H.; Szabó, Sándor

doi:10.1016/0014-4800(83)90099-0

Cited by 23 publications

(8 citation statements)

References 27 publications

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“…This endogeneous thiol compound is a substrate of an enzyme (glutathione peroxidase) which protects the cells from free radical reactions (4,17,32). This endogeneous thiol compound is a substrate of an enzyme (glutathione peroxidase) which protects the cells from free radical reactions (4,17,32).…”

Section: Discussionmentioning

confidence: 99%

Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts

et al. 1985

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Dog experiments were performed to describe the time course of lipid peroxidation after various ischemic influences of the heart measured by formation of malondialdehyde (MDA), and the scavenger action determined by reduced glutathione (GSH) content and superoxide dismutase (SOD) activity. Experimental groups consisted of control dogs having intact hearts and dogs with acute ramus descendens anterior ligature (LAD) having ischemic areas through 15, 30, 45 minutes and 1, 2, 3, 24 hours. Heart tissue for biochemical assays was excised from both the ischemic areas and from nonischemic left ventricle. The acute ischemia caused characteristic alterations in the biochemical parameters: MDA level gradually increased with its peak value being found at the end of 3 hours ligature. GSH levels decreased moderately, whereas SOD levels reduced sharply. As increased MDA formation indicates breakdown of the polyunsaturated fatty acids (PUFA) in the membranes and decreased GSH and SOD levels indicate impairment of the natural scavengering, the observed changes clearly outline the extent of disintegration of membrane structure and function.

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Section: Discussionmentioning

confidence: 99%

Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts

et al. 1985

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“…This sequence of ischemia and reperfusion results in liver damage due to I/R injury. Previous studies and our findings indicate that lipid peroxidation is the major cause of hepatic I/R injury [15][16][17]. Consequently, we compared three lipid mediators (F2-isoprostanes, 2-AG, and AEA) that sensitively reflect the progression of biomembrane damage with the conventional marker MDA.…”

Section: Discussionmentioning

confidence: 96%

F2-Isoprostanes and 2-Arachidonylglycerol as Biomarkers of Lipid Peroxidation in Pigs with Hepatic Ischemia/Reperfusion Injury

Ishii

Sakamoto

Ito

et al. 2010

Journal of Surgical Research

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“…Peroxidation of membrane phospholipids by oxygen-derived free radicals is a well-accepted mechanism of liver damage from toxic substances [5][6][7], and it has been logically assumed that the generation of free radicals during ischemia/reperfusion would cause cellular damage via similar mechanisms. However, recent studies have challenged this premise by failing to document the presence of free radicals or the products of lipid peroxidation in livers damaged by ischemia, even during reperfusion [13][14][15]. Each of these studies analyzed hepatocellular tissue fractions or whole liver tissue which was 70-92.5% hepatocytes by weight (32).…”

Section: Discussionmentioning

confidence: 99%

“…However, most of the support for this mechanism of irreversible cellular damage comes from models of hepatic injury involving alcohol [8], iron overload [9], paraquat and diquat [10], acetaminophen [11], and carbon tetrachloride [40]. In models of ischemic damage, the evidence is mixed; certain organ systems (e.g., brain mitochondria) support the role of lipid peroxidation [12], while many others do not (e.g., in situ canine heart and whole rat liver) [14,15].…”

Section: Introductionmentioning

confidence: 99%

Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

Walsh

Rao

Makowka

et al. 1990

Journal of Surgical Research

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A proposed mechanism for irreversible ischemic liver damage has been peroxidation of membrane phospholipids by free radicals. However, the hepatocyte is laden with enzymes which are antioxidants and, therefore, ought to be relatively resistant to oxidative injury. To test the hypothesis that free radical damage from ischemia and reperfusion of the liver is a non parenchymal cell process, we studied an in vivo model of ischemia. A point of transition from reversible to irreversible ischemia was defined at ≥60 min of total ischemia by serial measurements of ATP at control, end of ischemia, and end of reperfusion periods (n = 6 each). Nonparenchymal cells were separated out of 10 livers in each ischemic group using a Percoll gradient. Second derivative spectroscopy did not detect conjugated dienes in any hepatocellular fraction, total cellular, mitochondrial, or microsomal, but did in the nonparenchymal cell fractions of livers from the 60-and 90-min ischemia groups. This in vivo study shows that irreversible ischemia in the rat liver is associated with free radical lipid peroxidation, but that the non parenchymal cells rather than hepatocytes are the focus of this injury.

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Role of lipid peroxidation in tissue injury after hepatic ischemia

Cited by 23 publications

References 27 publications

Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts

Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts

F2-Isoprostanes and 2-Arachidonylglycerol as Biomarkers of Lipid Peroxidation in Pigs with Hepatic Ischemia/Reperfusion Injury

Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

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