Glebov A, Zinchuk V
Department of Physiology, Grodno State Medical University, Belarus.
Rocz Akad Med Bialymst. 2005;50:247-51.
Our aim was to study the blood oxygen-carrying function during the oxidative stress with a modification of the L-arginine-NO pathway.
Oxidative stress was induced by intravenous administration of Escherichia coli lipopolysaccharide (LPS) to rabbits. To modify the L-arginine-NO pathway, animals were administered with NG-nitro-L-arginine methyl ester intravenously 60 min after the LPS. Mixed venous blood was sampled for evaluation of blood oxygen transport before and at 120 and 240 min after the LPS administration; tissue samples (heart, lung, liver, kidney and muscle) were also prepared. The following parameters were measured hemoglobin-oxygen affinity, concentrations of conjugated dienes, Schiff bases, alpha-tocopherol and activity of catalase.
During the NO synthase inhibition the oxidative stress was characterized by a shift of hemoglobin oxygen dissociation curve rightwards, more prominent activation of lipid peroxidation and decreased tissue levels of antioxidant defense factors.
The inhibition of NO generation induces a shift of prooxidant-antioxidant balance--obviously, not only due its potentially high levels and reactivity with the various target molecules (with a development of oxidative stress), but also because of the lower contribution of other factors including the hemoglobin-oxygen affinity change into the body antioxidant potential.
我们的目的是通过改变L-精氨酸-一氧化氮途径来研究氧化应激期间的血液携氧功能。
通过给兔子静脉注射大肠杆菌脂多糖（LPS）诱导氧化应激。为改变L-精氨酸-一氧化氮途径，在注射LPS 60分钟后给动物静脉注射NG-硝基-L-精氨酸甲酯。在注射LPS前以及注射后120分钟和240分钟采集混合静脉血以评估血液氧运输；还制备了组织样本（心脏、肺、肝、肾和肌肉）。测量以下参数：血红蛋白-氧亲和力、共轭二烯浓度、席夫碱、α-生育酚以及过氧化氢酶活性。
在一氧化氮合酶抑制期间，氧化应激的特征是血红蛋白氧解离曲线向右移动、脂质过氧化更显著激活以及组织抗氧化防御因子水平降低。
一氧化氮生成的抑制导致促氧化剂-抗氧化剂平衡发生变化——显然，这不仅是由于其潜在的高水平以及与各种靶分子的反应性（伴随氧化应激的发展），还因为包括血红蛋白-氧亲和力变化在内的其他因素对机体抗氧化潜力的贡献较低。
