Effects of a hydroxyl radical scavenger, EPC-K1, and neutrophil depletion on reperfusion injury in rat skeletal muscle

Hirose, Jun; Yamaga, Makio; Kato, Teiji; Ikebe, Kenshiro; Takagi, Katsumasa

doi:10.1080/000164701753542078

Cited by 13 publications

(16 citation statements)

References 19 publications

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“…This was associated with diminished lipid peroxidation, protein oxidation, muscle cell membrane damage, and edema, clearly demonstrating the ability of neutrophils to cause oxidative damage and edema. Although no previous studies have measured tissue neutrophil levels after claudication or depleted neutrophils before claudication, our findings are in agreement with others showing attenuation of lipid peroxidation and edema (18) and reduction of muscle permeability (30) with neutrophil depletion before prolonged I/R.…”

Section: Discussionsupporting

confidence: 82%

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Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Judge

Dodd

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Judge, A. R., and S. L. Dodd. Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication. Am J Physiol Heart Circ Physiol 286: H252-H256, 2004. First published September 11, 2003 10.1152/ajpheart.00684. 2003.-We previously showed oxidative damage and edema within skeletal muscle after contractile claudication. To investigate the sources of this oxidative damage in the gastrocnemius muscle, we administered allopurinol (Allo, to inhibit xanthine oxidase) and cyclophosphamide (Cyclo, to deplete neutrophils) before inducing contractile claudication in male Sprague Dawley rats. Contractile claudication (ligated stimulated, LS) caused a significant increase in xanthine oxidase activity [sham ligated stimulated (SS) ϭ 2.57 Ϯ 0.07; LS ϭ 3.22 Ϯ 0.07] and neutrophil infiltration (SS ϭ 0.47 Ϯ 0.03; LS ϭ 0.91 Ϯ 0.10) compared with controls (SS), and this was associated with increased lipid peroxidation, protein oxidation, muscle damage, and edema. Pretreatment with Allo attenuated the increase in xanthine oxidase activity and attenuated lipid hydroperoxides (control LS ϭ 12.85 Ϯ 0.50; Allo LS ϭ 9.96 Ϯ 0.71), muscle damage, and neutrophil infiltration (control LS ϭ 0.91 Ϯ 0.10; Allo LS ϭ 0.61 Ϯ 0.07). This latter finding suggests that xanthine oxidasederived oxidants are chemotactic to neutrophils. Pretreatment with Cyclo reduced neutrophil infiltration (control LS ϭ 0.91 Ϯ 0.10; Cyclo LS ϭ 0.55 Ϯ 0.02) and attenuated lipid peroxidation (control LS ϭ 12.85 Ϯ 0.50; Cyclo LS ϭ 6.462 Ϯ 0.62), protein oxidation (control LS ϭ 2.59 Ϯ 0.47; Cyclo LS ϭ 1.77 Ϯ 0.60), muscle damage, and edema. Together, these data indicate that contractile claudication causes an increase in xanthine oxidase activity and neutrophils in muscle and that inhibition of these oxidant sources protects against oxidative stress, muscle damage, and edema. occlusion; free radicals; reactive oxygen species; muscle contraction SEVERAL STUDIES HAVE SHOWN that ischemia-reperfusion (I/R) caused by exercise claudication elevates markers of oxidative damage in the plasma. Hickman et al. (16) exercised claudicant patients for 10 min and found an increase in plasma malondialdehyde levels after exercise, whereas Silvestro et al. (32) showed an increase in thiobarbituric acid-reactive substances, as a marker of lipid peroxidation, after maximal, but not submaximal, exercise in claudicants.Likewise, markers of oxidative damage are also elevated in skeletal muscle after claudication. We recently found (21) an increase in protein oxidation and lipid peroxidation and a reduction in total glutathione levels 1 h after exercise with an animal model of claudication. This was associated with an increase in xanthine oxidase activity and neutrophils-both sources of oxidizing species.To further explore these findings and determine the relative contributions of each pathway, we chose to 1) inhibit xanthine oxidase activity and 2) deplete neutrophils and then measure markers of oxidative damage. Thus the purpose of this study wa...

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Section: Discussionsupporting

confidence: 82%

“…The dry weighing was terminated when the same weight was recorded three times in succession. The wet-to-dry ratio provides an index of edema formation (18).…”

Section: Methodsmentioning

confidence: 99%

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Judge

Dodd

2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Furthermore, several authors reported that skeletal muscle damage induced by I/R is largely dependent on ROS generation. 10,11 In agreement with data obtained in ischemic Zaccagnini et al p66 ShcA -Null Mice Are Resistant to Ischemia 2921 mice, it was found that tissue damage after hindlimb I/R was much lower in p66 ShcA Ϫ/Ϫ mice. Results obtained may be due to both decreased production and increased scavenging of ROS.…”

Section: Although the Role Of P66supporting

confidence: 80%

p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia

et al. 2004

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Background— Oxidative stress plays a pivotal role in ischemia and ischemia/reperfusion injury. Because p66 ShcA -null (p66 ShcA −/−) mice exhibit both lower levels of intracellular reactive oxygen species and increased resistance to cell death induced by oxidative stress, we investigated whether tissue damage that follows acute ischemia or ischemia/reperfusion was altered in p66 ShcA −/− mice. Methods and Results— Unilateral hindlimb ischemia was induced by femoral artery dissection, and ischemia/reperfusion was induced with an elastic tourniquet. Both procedures caused similar changes in blood perfusion in p66 ShcA wild-type (p66 ShcA wt) and p66 ShcA −/− mice. However, significant differences in tissue damage were found: p66 ShcA wt mice displayed marked capillary density decrease and muscle fiber necrosis. In contrast, in p66 ShcA −/− mice, minimal capillary density decrease and myofiber death were present. When apoptosis after ischemia was assayed, significantly lower levels of apoptotic endothelial cells and myofibers were found in p66 ShcA −/− mice. In agreement with these data, both satellite muscle cells and endothelial cells isolated from p66 ShcA −/− mice were resistant to apoptosis induced by simulated ischemia in vitro. Lower apoptosis levels after ischemia in p66 ShcA −/− cells correlated with decreased levels of oxidative stress both in vivo and in vitro. Conclusions— p66 ShcA plays a crucial role in the cell death pathways activated by acute ischemia and ischemia/reperfusion, indicating p66 ShcA as a potential therapeutic target for prevention and treatment of ischemic tissue damage.

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“…EPC-K1 is a phosphate diester of a-tocopherol and ascorbic acid, and has been reported to have an antioxidant effect by removing hydroxyl radicals and inhibiting phospholipase A2 [11]. It has also been reported to have a mitigating effect on I/R injury in the brain, heart, and skeletal muscles [12][13][14]. We previously showed that EPC-K1 has anti-inflammatory effects in a LPS-induced systemic inflammation model [15].…”

Section: Introductionmentioning

confidence: 99%

The Vitamin E Derivative, EPC-K1, Suppresses Inflammation During Hepatic Ischemia-Reperfusion Injury and Exerts Hepatoprotective Effects in Rats

Oishi

Hagiwara

Koga

et al. 2012

Journal of Surgical Research

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Effects of a hydroxyl radical scavenger, EPC-K1, and neutrophil depletion on reperfusion injury in rat skeletal muscle

Cited by 13 publications

References 19 publications

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia

The Vitamin E Derivative, EPC-K1, Suppresses Inflammation During Hepatic Ischemia-Reperfusion Injury and Exerts Hepatoprotective Effects in Rats

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Effects of a hydroxyl radical scavenger, EPC-K1, and neutrophil depletion on reperfusion injury in rat skeletal muscle

Cited by 13 publications

References 19 publications

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

p66 ShcA Modulates Tissue Response to Hindlimb Ischemia

The Vitamin E Derivative, EPC-K1, Suppresses Inflammation During Hepatic Ischemia-Reperfusion Injury and Exerts Hepatoprotective Effects in Rats

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Product

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p66 ^ShcA Modulates Tissue Response to Hindlimb Ischemia