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Resistance of erythrocytes to lipid peroxidation in cirrhotic rats.

机译:肝硬化大鼠红细胞对脂质过氧化的抗性。

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BACKGROUND: The aim of the present study was to investigate erythrocyte prooxidant-antioxidant balance in relation to liver and plasma lipid peroxidation in thioacetamide (TAA)-induced liver cirrhosis in rats. METHODS: Liver cirrhosis was produced by the administration of TAA (0.3 g/L of tap water) for a period of 3 months in rats. Serum, liver and erythrocyte lipid peroxide levels as well as liver glutathione (GSH) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined in cirrhotic rats. RESULTS: Hepatic cirrhosis was assessed by biochemical and histopathological findings. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities and malondialdehyde (MDA) levels increased in cirrhotic rats. This treatment caused increased MDA and diene conjugate (DC) levels as well as decreased GSH levels and GSH-Px activities in the liver of cirrhotic rats. In these conditions, no significant changes in erythrocyte cholesterol, phospholipid levels as well as endogenous DC, and GSH levels and spontaneous hemolysis values were observed in erythrocytes of rats with TAA-induced liver cirrhosis. However, H(2)O(2)-induced MDA levels were detected to decrease significantly in erythrocytes of cirrhotic rats. CONCLUSIONS: Our results indicate that erythrocytes of TAA-induced cirrhotic rats have a resistance against peroxidative stress in contrast to the findings in plasma and liver.
机译:背景:本研究的目的是研究与硫代乙酰胺(TAA)诱导的大鼠肝硬化的肝脏和血浆脂质过氧化有关的红细胞促氧化剂-抗氧化剂的平衡。方法:在大鼠中服用TAA(0.3 g / L自来水),持续3个月可引起肝硬化。测定了肝硬化大鼠的血清,肝和红细胞脂质过氧化物水平以及肝谷胱甘肽(GSH)水平和超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性。结果:通过生化和组织病理学检查评估了肝硬化。肝硬化大鼠血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)活性和丙二醛(MDA)水平升高。这种治疗导致肝硬化大鼠肝脏中的MDA和二烯共轭(DC)水平升高,以及GSH水平和GSH-Px活性降低。在这些情况下,在TAA诱发的肝硬化大鼠的红细胞中,未观察到红细胞胆固醇,磷脂水平以及内源性DC和GSH水平以及自发溶血值的显着变化。但是,H(2)O(2)诱导的丙二醛水平在肝硬化大鼠的红细胞中明显降低。结论:我们的结果表明,与血浆和肝脏中的发现相反,TAA诱导的肝硬化大鼠的红细胞具有抗过氧化应激的能力。

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