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抗坏血酸在拮抗大鼠三羟甲基氨基甲烷硝普钠肾毒性中的作用。

Role of ascorbic acid in counteracting ferric nitrilotriacetate-induced nephrotoxicity in rats.

机构信息

Department of Clinical Laboratory Sciences, College of Applied Medical Science, King Saud University , Riyadh , Saudi Arabia and.

出版信息

Pharm Biol. 2013 Dec;51(12):1559-63. doi: 10.3109/13880209.2013.802811. Epub 2013 Sep 12.

DOI:10.3109/13880209.2013.802811
PMID:24024952
Abstract

CONTEXT

Ascorbic acid (AA) is a naturally occurring organic compound with antioxidant properties. It is necessary for normal growth and development, and has been shown to protect against tissue toxicity and oxidative stress.

OBJECTIVE

The protective effect of AA against nephrotoxicity induced in albino rats by ferric nitrilotriacetate (Fe-NTA) was evaluated.

MATERIALS AND METHODS

Male albino rats of Wistar strain (4-6 weeks old) weighing 125-150 g were used in this study. Animals were given a single dose of Fe-NTA (9 mg/kg body weight, intraperitoneal) after a week of treatment with AA (1 and 2 mg/animal/day).

RESULTS

Fe-NTA treatment enhanced microsomal lipid peroxidation (LPO) and hydrogen peroxide (H2O2) generation to 1.7- to 2.2-fold, glutathione (GSH) levels were decreased by two-fold and the activities of GSH metabolizing enzymes decreased to a range of 2.2- to 2.5-fold in renal tissue. These changes were reversed significantly in animals receiving pretreatment of AA. Treatment of rats with AA prior to the treatment with Fe-NTA decreased microsomal LPO and H2O2 generation to 124 and 172%, and also resulted in the recovery of reduced levels of GSH, GSH-metabolizing enzymes to almost 92% at the higher dose level of AA.

DISCUSSION AND CONCLUSION

AA protects against Fe-NTA-induced nephrotoxicity and renal damage. AA has a beneficial impact on Fe-NTA-induced toxicity due to its scavenging and antioxidant effect in albino rats.

摘要

背景

抗坏血酸(AA)是一种具有抗氧化特性的天然有机化合物。它是正常生长和发育所必需的,已被证明可防止组织毒性和氧化应激。

目的

评估 AA 对三(2-羧乙基)膦盐酸盐(Fe-NTA)诱导的白化大鼠肾毒性的保护作用。

材料和方法

本研究使用 Wistar 品系雄性白化大鼠(4-6 周龄),体重 125-150g。动物在接受 AA(1 和 2mg/动物/天)治疗一周后,给予 Fe-NTA(9mg/kg 体重,腹腔内)单次剂量。

结果

Fe-NTA 处理使微粒体脂质过氧化(LPO)和过氧化氢(H2O2)生成增加 1.7-2.2 倍,谷胱甘肽(GSH)水平降低 2 倍,GSH 代谢酶活性降低 2.2-2.5 倍在肾组织中。在接受 AA 预处理的动物中,这些变化显著逆转。在给予 Fe-NTA 之前用 AA 处理大鼠,可使微粒体 LPO 和 H2O2 生成减少 124%和 172%,并使还原型 GSH 和 GSH 代谢酶的水平恢复到较高剂量 AA 时的近 92%。

讨论与结论

AA 可防止 Fe-NTA 诱导的肾毒性和肾损伤。AA 具有清除和抗氧化作用,对 Fe-NTA 诱导的毒性具有有益影响。

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