2008
DOI: 10.1152/ajpheart.00378.2007
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In vivo reactive oxygen species production induced by ischemia in muscle arterioles of mice: involvement of xanthine oxidase and mitochondria

Abstract: Reactive oxygen species (ROS) participate in tissue injury after ischemia-reperfusion. Their implication in leukocyte adherence and increase in permeability at the venular side of the microcirculation have been reported, but very little is known about ROS production in arterioles. The objective of this work was to evaluate, in the arteriole wall in vivo, the temporal changes in superoxide anion production during ischemia and reperfusion and to identify the source of this production. Mouse cremaster muscle was … Show more

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Cited by 60 publications
(32 citation statements)
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“…During ischemia, xanthine dehydrogenase, which is found in the microvascular endothelial cells of skeletal muscle, is converted to XO (189), which, in turn, catalyzes the conversion of hypoxanthine to xanthine by producing O 2 ·Ϫ . Thus the primary sources of ROS during ischemia seem to be XO and mitochondrial complexes I and III (8,154,184). Skeletal muscle contains 10 -15% of the body's iron stores, mainly in mitochondria and myoglobin (7).…”
Section: Chronology Of Events At the Level Of Skeletal Muscle Fiber Cmentioning
confidence: 99%
See 1 more Smart Citation
“…During ischemia, xanthine dehydrogenase, which is found in the microvascular endothelial cells of skeletal muscle, is converted to XO (189), which, in turn, catalyzes the conversion of hypoxanthine to xanthine by producing O 2 ·Ϫ . Thus the primary sources of ROS during ischemia seem to be XO and mitochondrial complexes I and III (8,154,184). Skeletal muscle contains 10 -15% of the body's iron stores, mainly in mitochondria and myoglobin (7).…”
Section: Chronology Of Events At the Level Of Skeletal Muscle Fiber Cmentioning
confidence: 99%
“…The possible mechanisms described in the literature are 1) a mitochondrial membrane depolarization that triggers mPTP opening and 2) opening of a mitochondrial inner membrane anion channel (57,205). Other potential important sources of free radical generation at reperfusion include NADPH oxidases, NO synthases, and XO (8,57,83,86,98). However, even if some reports suggest that mitochondria could not be a predominant source of ROS (76), activation of these processes seems to require an initial burst of mitochondrial ROS and contributes to secondary tissue damage and inflammation (31).…”
Section: ϩmentioning
confidence: 99%
“…To evaluate the effect of the specific mitochondrial complex II inhibitor thenoyltrifluoroacetone (TTFA, Sigma-Aldrich Chemical Corp., MO, U.S.A.), arterial sections were pre-incubated with Krebs-Henseleit buffer solution in a CO 2 incubator for 40 min at 37°C in the presence or absence of TTFA (10 µM). 21,22) Dihydroethidium fluorescence intensity in the segment was then measured using a confocallaser-scanning microscope system (as described above).…”
Section: Investigation Of Superoxide Production and Modulationmentioning
confidence: 99%
“…However, there is a discrepancy regarding whether ROS generation peaks during ischemia or during reperfusion. 64 In renal IRI, cellular ROS generation before, during, and after ischemia has not been investigated in real time. We therefore injected the superoxide-sensitive dye dihydroethidium (DHE) into an anaesthetized rat and imaged renal ROS production in vivo.…”
Section: Epithelial Dysfunctionmentioning
confidence: 99%