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叔丁基对苯二酚对次氮基三乙酸铁诱导的大鼠肝毒性和氧化应激的改善作用。

Ameliorative effect of butylated hydroxyanisole against ferric nitrilotriacetate-induced hepatotoxicity and oxidative stress in rats.

作者信息

Ansar S, Iqbal M

机构信息

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

Biotechnology Research Institute, Universiti Malaysia Sabah, Kota Kinabalu Sabah, Malaysia.

出版信息

Toxicol Ind Health. 2015 Nov;31(11):967-73. doi: 10.1177/0748233714554409. Epub 2014 Nov 20.

DOI:10.1177/0748233714554409
PMID:26499990
Abstract

Ferric nitrilotriacetate (Fe-NTA) is a known renal carcinogen and has been shown to adversely induce oxidative stress and tissue toxicity after both acute and chronic exposure. Present studies were designed to study the hepatoprotective and antioxidant potential of butylated hydroxyanisole (BHA), a phenolic antioxidant used in foods on ferric nitrilotriacetate (Fe-NTA) induced hepatotoxicity in rats. 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's treatment with BHA. BHA was administered orally once daily for 7 days at doses of 1 and 2 mg/animal/day. The hepatoprotective activity was assessed using various biochemical parameters as serum transaminases (alanine transaminase (ALT), aspartate transaminase (AST)) and lactate dehydrogenase (LDH). Fe-NTA treatment increased ALT, AST, and LDH levels significantly when compared to the corresponding saline-treated group (p < 0.001). Fe-NTA also depleted the levels of glutathione and the activities of antioxidant enzymes namely glutathione reductase and glutathione-S-tranferase (p < 0.05). Pretreatment with BHA significantly decreased ALT, AST and LDH levels in a dose-dependent manner (p < 0.05). BHA also increased antioxidant enzymes level and decreased lipid peroxidation and hydrogen peroxide generation to 1.3-1.5-fold as compared to Fe-NTA-treated group. The results show the strong hepatoprotective activity of BHA which could be due to its potent antioxidant effects.

摘要

次氮基三乙酸铁(Fe-NTA)是一种已知的肾致癌物,已表明在急性和慢性暴露后均会不利地诱导氧化应激和组织毒性。目前的研究旨在研究食品中使用的酚类抗氧化剂丁基化羟基茴香醚(BHA)对次氮基三乙酸铁(Fe-NTA)诱导的大鼠肝毒性的肝保护和抗氧化潜力。本研究使用了体重125-150g的Wistar品系雄性白化大鼠(4-6周龄)。在用BHA治疗一周后,给动物单次注射Fe-NTA(9mg/kg体重,腹腔注射)。BHA以1和2mg/动物/天的剂量口服给药,每天一次,共7天。使用各种生化参数如血清转氨酶(丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST))和乳酸脱氢酶(LDH)评估肝保护活性。与相应的生理盐水处理组相比,Fe-NTA处理显著提高了ALT、AST和LDH水平(p<0.001)。Fe-NTA还降低了谷胱甘肽水平以及抗氧化酶即谷胱甘肽还原酶和谷胱甘肽-S-转移酶的活性(p<0.05)。用BHA预处理以剂量依赖方式显著降低了ALT、AST和LDH水平(p<0.05)。与Fe-NTA处理组相比,BHA还使抗氧化酶水平升高,并使脂质过氧化和过氧化氢生成降低至1.3-1.5倍。结果显示BHA具有强大的肝保护活性,这可能归因于其强大的抗氧化作用。

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