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肝硬化大鼠红细胞对脂质过氧化的抗性

Resistance of erythrocytes to lipid peroxidation in cirrhotic rats.

作者信息

Oztezcan Serdar, Balkan Jale, Dogru-Abbasoglu Semra, Cevikbas Ugur, Aykaç-Toker Gülçin, Uysal Müjdat

机构信息

Department of Biochemistry, University of Istanbul, Turkey.

出版信息

Arch Med Res. 2005 Sep-Oct;36(5):459-63. doi: 10.1016/j.arcmed.2005.03.044.

Abstract

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.

摘要

背景

本研究旨在探讨硫代乙酰胺(TAA)诱导的大鼠肝硬化中红细胞促氧化剂-抗氧化剂平衡与肝脏及血浆脂质过氧化的关系。

方法

通过给大鼠饮用含0.3 g/L TAA的自来水3个月来诱导肝硬化。测定肝硬化大鼠血清、肝脏和红细胞脂质过氧化物水平以及肝脏谷胱甘肽(GSH)水平、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肝硬化情况。肝硬化大鼠血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)活性及丙二醛(MDA)水平升高。该处理导致肝硬化大鼠肝脏中MDA和二烯共轭物(DC)水平升高,同时GSH水平和GSH-Px活性降低。在这些情况下,TAA诱导的肝硬化大鼠红细胞中胆固醇、磷脂水平以及内源性DC、GSH水平和自发溶血值均未观察到显著变化。然而,检测发现肝硬化大鼠红细胞中H₂O₂诱导的MDA水平显著降低。

结论

我们的结果表明,与血浆和肝脏中的情况相反,TAA诱导的肝硬化大鼠红细胞对过氧化应激具有抗性。

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