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抗坏血酸对大鼠肝脏缺血/再灌注损伤的体内细胞保护作用。

The in vivo cytoprotection of ascorbic acid against ischemia/reoxygenation injury of rat liver.

作者信息

Ozaki M, Fuchinoue S, Teraoka S, Ota K

机构信息

Department of Surgery III, Tokyo Women's Medical College, Japan.

出版信息

Arch Biochem Biophys. 1995 Apr 20;318(2):439-45. doi: 10.1006/abbi.1995.1252.

DOI:10.1006/abbi.1995.1252
PMID:7733675
Abstract

The in vivo effects of ascorbic acid on the reoxygenated liver tissue were examined, with regard to the following effects: (i) the effects of scavenging radicals and/or reducing peroxidative reactions, and (ii) the effects of the chelation with low-molecular-weight iron and increasing its reactivity (radical production). Ascorbic acid is one of the water-soluble vitamins known to have various physiological effects involving both chelating and reducing properties at once. Lipid peroxidation of the reoxygenated liver tissue estimated by the production of TBARS (thiobarbituric acid-reactive substance) and LPO (lipid hydroperoxides) was suppressed effectively by the preischemic intraperitoneal administration of ascorbic acid. Ascorbic acid also showed this anti-oxidant effect in a dose-dependent manner. The analysis of the levels of ascorbic acid and glutathione of the liver tissue revealed that ascorbic acid works as an anti-oxidant probably by being oxydized finally to dehydroascorbic acid just after the reoxygenation. The latter was reduced to ascorbic acid again, coupled with the conversion of GSH to GSSG in the postischemic time course. The predominant effect of ascorbic acid on the reoxygenated liver tissue seems to be caused by the scavenging radicals and/or reducing peroxidative reactions, rather than by chelating iron and increasing its reactivity (radical production). Cellular integrity (estimated by the release of GOT, GPT, and LDH) and the energy state of the postischemic liver tissue (estimated by the tissue ATP level) were also well preserved by the administration of ascorbic acid.

摘要

研究了抗坏血酸对复氧肝组织的体内作用,涉及以下方面:(i)清除自由基和/或减少过氧化反应的作用,以及(ii)与低分子量铁螯合并增加其反应性(自由基产生)的作用。抗坏血酸是一种水溶性维生素,已知具有多种生理作用,同时具有螯合和还原特性。通过丙二醛(硫代巴比妥酸反应性物质)和脂质氢过氧化物的产生来估计复氧肝组织的脂质过氧化,结果表明,缺血前腹腔注射抗坏血酸可有效抑制这种脂质过氧化。抗坏血酸还呈剂量依赖性地表现出这种抗氧化作用。对肝组织中抗坏血酸和谷胱甘肽水平的分析表明,抗坏血酸可能通过在复氧后最终氧化为脱氢抗坏血酸而发挥抗氧化剂的作用。在缺血后的时间进程中,后者再次还原为抗坏血酸,同时谷胱甘肽转化为氧化型谷胱甘肽。抗坏血酸对复氧肝组织的主要作用似乎是由清除自由基和/或减少过氧化反应引起的,而不是通过螯合铁并增加其反应性(自由基产生)。给予抗坏血酸还能很好地维持细胞完整性(通过谷草转氨酶、谷丙转氨酶和乳酸脱氢酶的释放来估计)和缺血后肝组织的能量状态(通过组织三磷酸腺苷水平来估计)。

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