Rajeswari Arjunan, Varalakshmi Palaninathan
Department of Medical Biochemistry, Dr. AL Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai-600 113, India.
Clin Chim Acta. 2006 Aug;370(1-2):108-14. doi: 10.1016/j.cca.2006.01.027. Epub 2006 Mar 3.
Oxidative stress has emerged as an invariable feature of calculogenesis, the process of stone formation. The cytoprotective action of low molecular weight heparin (LMWH) in calcium oxalate-induced oxidative renal injury in experimental calculogenesis was studied.
A renal membrane injury model involving gentamicin (40 mg/kg body weight) and 2% ammonium oxalate was used. Rats induced with gentamicin and ammonium oxalate were investigated for any impairment of cellular redox status as revealed by renal superoxide dismutase, catalase, glutathione peroxidase, xanthine oxidase activities and glutathione, ascorbate levels. In renal membrane protein activities such as aminotransferases in kidney and lactate dehydrogenase, total protein in urine of rats rendered lithogenic were assessed and compared with healthy vehicle-treated controls. The biochemical index of tissue lipid peroxidation was assessed in terms of malondialdehyde formation. LMWH was co-administered (250 microg/kg body weight) to gentamicin- and ammonium oxalate-dosed rats.
The extent of oxidative damage was indicated by the increased lipid peroxidation in the renal tissues of gentamicin- and ammonium oxalate-administered groups. The decline in the antioxidative status of the stone forming kidneys further confirmed the oxidative stress to renal cells. The extensive nephritic damage in the form of proteinuria was quite evident and the injured status of the tissue was reflected in the significant alterations of the few membrane associated enzyme levels in urine and the kidney. LMWH restricted all the cyto-oxidative ill effects of ammonium oxalate and gentamicin.
Low molecular weight heparin has antioxidant potential in countering the oxalate/calcium oxalate-mediated oxidative challenge in the experimental lithogenic model.
氧化应激已成为结石形成过程（即结石生成过程）中一个不变的特征。研究了低分子量肝素（LMWH）在实验性结石生成中对草酸钙诱导的氧化性肾损伤的细胞保护作用。
采用庆大霉素（40mg/kg体重）和2%草酸铵诱导的肾膜损伤模型。研究了用庆大霉素和草酸铵诱导的大鼠的细胞氧化还原状态的任何损害，这可通过肾超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、黄嘌呤氧化酶活性以及谷胱甘肽、抗坏血酸水平来揭示。评估了致石大鼠肾脏中氨基转移酶等肾膜蛋白活性以及乳酸脱氢酶、尿总蛋白，并与健康的赋形剂处理对照组进行比较。根据丙二醛的形成评估组织脂质过氧化的生化指标。将LMWH（250μg/kg体重）与庆大霉素和草酸铵给药的大鼠联合给药。
庆大霉素和草酸铵给药组肾组织中脂质过氧化增加表明氧化损伤程度。结石形成肾脏的抗氧化状态下降进一步证实了对肾细胞的氧化应激。蛋白尿形式的广泛肾损伤非常明显，组织的损伤状态反映在尿液和肾脏中少数膜相关酶水平的显著改变上。LMWH限制了草酸铵和庆大霉素的所有细胞氧化不良影响。
在实验性结石生成模型中，低分子量肝素具有抗氧化潜力，可对抗草酸盐/草酸钙介导的氧化挑战。
