Effect of vitamin E on reoxygenation injury experienced by isolated rat hepatocytes

Paolo Caraceni; Tony Yao; Silvia Degli Esposti; Antonio Gasbarrini; Brian T. Bowie; Mark A Zern; Andre B. Borle; David H. Van Thiel

doi:10.1016/0024-3205(94)00757-8

Effect of vitamin E on reoxygenation injury experienced by isolated rat hepatocytes

Paolo Caraceni, Tony Yao, Silvia Degli Esposti, Antonio Gasbarrini, Brian T. Bowie, Mark A Zern, Andre B. Borle, David H. Van Thiel

Research output: Contribution to journal › Article

15 Scopus citations

Abstract

The pathogenic role of lipid peroxidation in the reperfusion injury of the liver is still controversial. This study was performed to determine whether the damage caused by oxygen free radicals during reoxygenation in perfused rat hepatocytes is related to lipid peroxidation. Superoxide anion was detected by lucigenin-enhanced chemiluminescence. Lipid peroxidation and cell injury were assessed by the release of malondialdehyde and lactic dehydrogenase. Upon reoxygenation following 2.5 h of anoxia, isolated hepatocytes generated considerable amount of O_2-. Following O_2- formation, a significant increase in malondialdehyde release was measured. Cell injury was temporally delayed relative to O_2- generation, but preceded the occurence of a significant lipid peroxidation. Treatment with Vitamin E abolished lipid peroxidation but had no effect upon superoxide anion formation and cell injury. These results suggest that in perfused rat hepatocytes non-peroxidative mechanisms are more important than peroxidative mechanisms in the pathogenesis of the early phases of reoxygenation injury.

Original language	English (US)
Pages (from-to)	1427-1432
Number of pages	6
Journal	Life Sciences
Volume	55
Issue number	18
DOIs	https://doi.org/10.1016/0024-3205(94)00757-8
State	Published - 1994
Externally published	Yes

Keywords

lipid peroxidation
oxygen free radicals
reoxygenation injury
vitamin E

ASJC Scopus subject areas

Pharmacology

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Caraceni, P., Yao, T., Esposti, S. D., Gasbarrini, A., Bowie, B. T., Zern, M. A., Borle, A. B., & Van Thiel, D. H. (1994). Effect of vitamin E on reoxygenation injury experienced by isolated rat hepatocytes. Life Sciences, 55(18), 1427-1432. https://doi.org/10.1016/0024-3205(94)00757-8

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title = "Effect of vitamin E on reoxygenation injury experienced by isolated rat hepatocytes",

abstract = "The pathogenic role of lipid peroxidation in the reperfusion injury of the liver is still controversial. This study was performed to determine whether the damage caused by oxygen free radicals during reoxygenation in perfused rat hepatocytes is related to lipid peroxidation. Superoxide anion was detected by lucigenin-enhanced chemiluminescence. Lipid peroxidation and cell injury were assessed by the release of malondialdehyde and lactic dehydrogenase. Upon reoxygenation following 2.5 h of anoxia, isolated hepatocytes generated considerable amount of O2-. Following O2- formation, a significant increase in malondialdehyde release was measured. Cell injury was temporally delayed relative to O2- generation, but preceded the occurence of a significant lipid peroxidation. Treatment with Vitamin E abolished lipid peroxidation but had no effect upon superoxide anion formation and cell injury. These results suggest that in perfused rat hepatocytes non-peroxidative mechanisms are more important than peroxidative mechanisms in the pathogenesis of the early phases of reoxygenation injury.",

keywords = "lipid peroxidation, oxygen free radicals, reoxygenation injury, vitamin E",

author = "Paolo Caraceni and Tony Yao and Esposti, {Silvia Degli} and Antonio Gasbarrini and Bowie, {Brian T.} and Zern, {Mark A} and Borle, {Andre B.} and {Van Thiel}, {David H.}",

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AU - Caraceni, Paolo

AU - Yao, Tony

AU - Esposti, Silvia Degli

AU - Gasbarrini, Antonio

AU - Bowie, Brian T.

AU - Zern, Mark A

AU - Borle, Andre B.

AU - Van Thiel, David H.

PY - 1994

Y1 - 1994

N2 - The pathogenic role of lipid peroxidation in the reperfusion injury of the liver is still controversial. This study was performed to determine whether the damage caused by oxygen free radicals during reoxygenation in perfused rat hepatocytes is related to lipid peroxidation. Superoxide anion was detected by lucigenin-enhanced chemiluminescence. Lipid peroxidation and cell injury were assessed by the release of malondialdehyde and lactic dehydrogenase. Upon reoxygenation following 2.5 h of anoxia, isolated hepatocytes generated considerable amount of O2-. Following O2- formation, a significant increase in malondialdehyde release was measured. Cell injury was temporally delayed relative to O2- generation, but preceded the occurence of a significant lipid peroxidation. Treatment with Vitamin E abolished lipid peroxidation but had no effect upon superoxide anion formation and cell injury. These results suggest that in perfused rat hepatocytes non-peroxidative mechanisms are more important than peroxidative mechanisms in the pathogenesis of the early phases of reoxygenation injury.

AB - The pathogenic role of lipid peroxidation in the reperfusion injury of the liver is still controversial. This study was performed to determine whether the damage caused by oxygen free radicals during reoxygenation in perfused rat hepatocytes is related to lipid peroxidation. Superoxide anion was detected by lucigenin-enhanced chemiluminescence. Lipid peroxidation and cell injury were assessed by the release of malondialdehyde and lactic dehydrogenase. Upon reoxygenation following 2.5 h of anoxia, isolated hepatocytes generated considerable amount of O2-. Following O2- formation, a significant increase in malondialdehyde release was measured. Cell injury was temporally delayed relative to O2- generation, but preceded the occurence of a significant lipid peroxidation. Treatment with Vitamin E abolished lipid peroxidation but had no effect upon superoxide anion formation and cell injury. These results suggest that in perfused rat hepatocytes non-peroxidative mechanisms are more important than peroxidative mechanisms in the pathogenesis of the early phases of reoxygenation injury.

KW - lipid peroxidation

KW - oxygen free radicals

KW - reoxygenation injury

KW - vitamin E

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