Gündüz Filiz, Sentürk Umit Kemal
Department of Physiology, Medical Faculty, Akdeniz University, Kampus, 07070 Antalya, Turkey.
Eur J Appl Physiol. 2003 Nov;90(5-6):526-32. doi: 10.1007/s00421-003-0888-1. Epub 2003 Aug 2.
Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. We investigated whether free radicals generated during exercise play a role in post-exercise proteinuria in sedentary and treadmill-running trained rats, separately. Sedentary and trained rats were randomly divided into four sub-groups: control, antioxidant treatment, exhaustive exercise and an exhaustive exercise plus antioxidant treatment group. Antioxidant therapy was applied by intragastric catheter for 4 weeks with vitamin C (ascorbic acid, 50 mg x kg(-1) x day(-1)) and vitamin E (alpha-tocopherol, 20 mg x kg(-1).day(-1)). Twenty-four-hour urine samples were used for measuring protein levels and protein electrophoresis. Thiobarbituric acid (TBARS) and glutathione (GSH) levels, superoxide dismutase (SOD) and catalase (CAT) activities were assayed in blood and tissues. Increased urinary protein levels and mixed type proteinuria in electrophoresis were identified after exhaustive exercise in sedentary rats. Erythrocyte, kidney and muscle TBARS levels were significantly elevated in this group. Antioxidant treatment prevented the increase in urinary protein levels, TBARS levels and the occurrence of mixed type proteinuria after exhaustive exercise in sedentary rats. Exhaustive exercise in trained rats resulted in elevation of urine protein levels and mixed type proteinuria although kidney TBARS levels were not changed compared to those of the trained controls. Antioxidant therapy in trained and exhausted-trained animals resulted in decreased TBARS levels in the kidney but it did not affect urinary-increased protein levels or electrophoresis in exhausted animals. This findings suggest that the exercise-induced oxidant stress may contribute to post-exercise proteinuria in sedentary rats. However, this mechanism may not be responsible for proteinuria in trained rats.
运动性蛋白尿是身体活动的常见后果,但其机制尚不清楚。我们分别研究了运动过程中产生的自由基是否在久坐不动的大鼠和跑步机训练的大鼠运动后蛋白尿中起作用。将久坐不动的大鼠和训练有素的大鼠随机分为四个亚组:对照组、抗氧化剂治疗组、力竭运动组和力竭运动加抗氧化剂治疗组。通过胃管给予抗氧化剂治疗4周,使用维生素C(抗坏血酸,50 mg·kg⁻¹·d⁻¹)和维生素E(α-生育酚,20 mg·kg⁻¹·d⁻¹)。收集24小时尿液样本用于测量蛋白质水平和进行蛋白质电泳。测定血液和组织中的硫代巴比妥酸(TBARS)和谷胱甘肽(GSH)水平、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性。久坐不动的大鼠力竭运动后,尿蛋白水平升高,电泳显示为混合型蛋白尿。该组红细胞、肾脏和肌肉的TBARS水平显著升高。抗氧化剂治疗可预防久坐不动的大鼠力竭运动后尿蛋白水平升高、TBARS水平升高以及混合型蛋白尿的发生。训练有素的大鼠力竭运动导致尿蛋白水平升高和混合型蛋白尿,尽管与训练对照组相比,肾脏TBARS水平没有变化。训练有素且力竭运动的动物接受抗氧化剂治疗后,肾脏中的TBARS水平降低,但对力竭运动动物尿液中升高的蛋白质水平或电泳结果没有影响。这些发现表明,运动诱导的氧化应激可能导致久坐不动的大鼠运动后蛋白尿。然而,这种机制可能与训练有素的大鼠蛋白尿无关。