Tripathi Pratima, Pandey Shivani
Department of Biochemistry, University of Lucknow, Lucknow, India.
Indian J Biochem Biophys. 2013 Apr;50(2):99-104.
Increased production of oxygen free radicals and decreased oxidant capacity occur in coronary artery diseases (CAD) This pro-oxidant shift in intracellular redox state may induce cell death by either direct cell membrane damage by lipic peroxidation or apoptosis through activation of transcription factors. These changes occur not only in cardiomyocytes, bu also in cardiac sympathetic nerves, which are very sensitive to oxidative damage. Patients with heart failure encountel reduced peripheralblood flow at rest, during exercise and in response to endothelium-dependentvasodilators. Current treatments of cardiomyopathy, a degenerative condition of the myocardium frequently associated with heart failure have done little to enhance patient survival. Decreased myocardial contractility and altered regulation of peripheral circulation along with oxidative conditions are important contributors to the symptoms and prognosis of the disease process. Nitric oxide formed from L-arginine (2-amino-5 guanidinovaleric acid) metabolism in endothelial cells contributes to regulation of blood flow under these conditions. L-Arginine is the precursor of nitric oxide, an endogenous messenger molecule involved in a variety of endothelium-mediated physiological effects in the vascular system. In the present study, we investigated the effect of oral administration of L-arginine (3 g/day) on the intracellular redox status of the patients of ischemic cardiomyopathy aged 45-60 yrs. The enzymatic and non-enzymatic antioxidant parameters like superoxide dismutase, catalase, total thiols (TSH) and ascorbic acid along with pro-oxidant parameters, such as xanthine oxidase, as well as index of oxidative stress as protein carbonyl content and malondialdehyde (a marker of lipid peroxidation) were investigated in the plasma and RBC lysate. L-Arginine (3 g/day) administration was found to improve the levels of these parameters in the patients and regulate the blood flow, as evident by the improved blood pressure of the patients. Thus, it is inferred that L-arginine attenuates the oxidative stress conditions along with maintaining the blood pressure rate of patients suffering from cardiomyopathy.
冠状动脉疾病(CAD)中会出现氧自由基生成增加和氧化能力下降的情况。细胞内氧化还原状态的这种促氧化转变可能通过脂质过氧化直接损伤细胞膜或通过激活转录因子诱导细胞凋亡,从而导致细胞死亡。这些变化不仅发生在心肌细胞中,也发生在对氧化损伤非常敏感的心脏交感神经中。心力衰竭患者在静息、运动以及对内皮依赖性血管扩张剂作出反应时,外周血流量都会减少。心肌病是一种常与心力衰竭相关的心肌退行性疾病,目前针对心肌病的治疗在提高患者生存率方面收效甚微。心肌收缩力下降、外周循环调节改变以及氧化状态是导致该疾病进程症状和预后的重要因素。在内皮细胞中,由L-精氨酸(2-氨基-5-胍基戊酸)代谢形成的一氧化氮有助于在这些情况下调节血流。L-精氨酸是一氧化氮的前体,一氧化氮是一种内源性信使分子,参与血管系统中多种内皮介导的生理效应。在本研究中,我们调查了口服L-精氨酸(3克/天)对45至60岁缺血性心肌病患者细胞内氧化还原状态的影响。在血浆和红细胞裂解物中研究了超氧化物歧化酶、过氧化氢酶、总硫醇(TSH)和抗坏血酸等酶促和非酶促抗氧化参数,以及黄嘌呤氧化酶等促氧化参数,还有作为氧化应激指标的蛋白质羰基含量和丙二醛(脂质过氧化的标志物)。结果发现,给予L-精氨酸(3克/天)可改善患者这些参数的水平并调节血流,患者血压的改善就是明证。因此,可以推断L-精氨酸可减轻心肌病患者遭受的氧化应激状况,同时维持其血压水平。