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首页> 外文期刊>American Journal of Physiology >Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication.
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Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication.

机译：黄嘌呤氧化酶和活化的中性粒细胞在收缩性c行后对骨骼肌造成氧化损伤。

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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) = 2.57 +/- 0.07; LS = 3.22 +/- 0.07] and neutrophil infiltration (SS = 0.47 +/- 0.03; LS = 0.91 +/- 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 = 12.85 +/- 0.50; Allo LS = 9.96 +/- 0.71), muscle damage, and neutrophil infiltration (control LS = 0.91 +/- 0.10; Allo LS = 0.61 +/- 0.07). This latter finding suggests that xanthine oxidase-derived oxidants are chemotactic to neutrophils. Pretreatment with Cyclo reduced neutrophil infiltration (control LS = 0.91 +/- 0.10; Cyclo LS = 0.55 +/- 0.02) and attenuated lipid peroxidation (control LS = 12.85 +/- 0.50; Cyclo LS = 6.462 +/- 0.62), protein oxidation (control LS = 2.59 +/- 0.47; Cyclo LS = 1.77 +/- 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.
机译：收缩性lau行后，我们先前显示了骨骼肌内的氧化损伤和水肿。为了研究腓肠肌这种氧化损伤的来源，我们在雄性Sprague Dawley大鼠中诱发收缩性lau行之前，先给予了别嘌呤醇（Allo，以抑制黄嘌呤氧化酶）和环磷酰胺（Cyclo，以消耗中性粒细胞）。收缩性lau行（连接刺激，LS）导致黄嘌呤氧化酶活性显着增加[假连接刺激（SS）= 2.57 +/- 0.07; LS = 3.22 +/- 0.07]和中性粒细胞浸润（SS = 0.47 +/- 0.03; LS = 0.91 +/- 0.10），与对照组（SS）相比，这与脂质过氧化，蛋白质氧化，肌肉损伤，和水肿。用Allo预处理减弱了黄嘌呤氧化酶活性的增加，减弱了脂质氢过氧化物（对照LS = 12.85 +/- 0.50; Allo LS = 9.96 +/- 0.71），肌肉损伤和中性粒细胞浸润（对照LS = 0.91 +/- 0.10; Allo LS = 0.61 +/- 0.07）。后一个发现表明黄嘌呤氧化酶衍生的氧化剂对嗜中性粒细胞具有趋化性。用Cyclo预处理可减少中性粒细胞浸润（对照LS = 0.91 +/- 0.10; Cyclo LS = 0.55 +/- 0.02）和减弱的脂质过氧化作用（对照LS = 12.85 +/- 0.50; Cyclo LS = 6.462 +/- 0.62），蛋白质氧化（对照LS = 2.59 +/- 0.47; Cyclo LS = 1.77 +/- 0.60），肌肉损伤和水肿。总之，这些数据表明收缩性lau行导致肌肉中黄嘌呤氧化酶活性和中性粒细胞增加，并且抑制这些氧化剂可防止氧化应激，肌肉损伤和水肿。

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