Veena Coothan Kandaswamy, Josephine Anthony, Preetha Sreenivasan P, Varalakshmi Palaninathan, Sundarapandiyan Rajaguru
Department of Medical Biochemistry, Dr ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, India.
Life Sci. 2006 Oct 4;79(19):1789-95. doi: 10.1016/j.lfs.2006.06.014. Epub 2006 Jun 16.
Oxalate, one of the major constituents of renal stones is known to induce free radicals which damage the renal membrane. Damaged epithelia might act as nidi for stone formation aggravating calcium oxalate precipitation during hyperoxaluria. In the present study, the beneficial effects of fucoidan on oxalate-induced free radical injury were investigated. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two groups by administration of 0.75% ethylene glycol in drinking water for 28 days and one of them was treated with fucoidan from Fucus vesiculosus at a dose of 5 mg/kg b.wt subcutaneously commencing from the 8th day of induction. A control and drug control (fucoidan alone) was also included in the study. The extent of renal injury in hyperoxaluria was evident from the increased activities of alkaline phosphatase, gamma-glutamyl transferase, beta-glucuronidase, N-acetyl-beta-D-glucosaminidase in urine. There was a positive correlation between plasma malondialdehyde levels and renal membrane damage indicating a striking relation between free radical formation and cellular injury. Increased protein carbonyl and decreased thiols further exemplified the oxidative milieu prevailing during hyperoxaluria. Decreased renal membrane ATPases accentuated the renal membrane damage induced by oxalate. Renal microscopic analysis showed abnormal findings in histology as an evidence of oxalate damage. The above biochemical and histopathological discrepancies were abrogated with fucoidan administration, indicating its protective role in oxalate mediated peroxidative injury.
草酸盐是肾结石的主要成分之一,已知其可诱导自由基,从而损伤肾膜。受损的上皮细胞可能成为结石形成的核心,在高草酸尿症期间加重草酸钙沉淀。在本研究中,研究了岩藻依聚糖对草酸盐诱导的自由基损伤的有益作用。将雄性Wistar大鼠分为四组。两组通过在饮用水中给予0.75%乙二醇28天诱导高草酸尿症,其中一组从诱导的第8天开始皮下注射剂量为5mg/kg体重的墨角藻岩藻依聚糖进行治疗。研究中还包括一个对照组和药物对照组(仅岩藻依聚糖)。从尿中碱性磷酸酶、γ-谷氨酰转移酶、β-葡萄糖醛酸酶、N-乙酰-β-D-氨基葡萄糖苷酶活性增加可明显看出高草酸尿症中肾损伤的程度。血浆丙二醛水平与肾膜损伤呈正相关,表明自由基形成与细胞损伤之间存在显著关系。蛋白质羰基增加和硫醇减少进一步例证了高草酸尿症期间普遍存在的氧化环境。肾膜ATP酶减少加剧了草酸盐诱导的肾膜损伤。肾脏显微镜分析显示组织学上有异常发现,作为草酸盐损伤的证据。给予岩藻依聚糖可消除上述生化和组织病理学差异,表明其在草酸盐介导的过氧化损伤中的保护作用。