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丁羟甲苯对硝酸铁所致大鼠肾增生和损伤的抗氧化作用。

Antioxidant effect of butylated hydroxytoluene on ferric nitrilotriacetate induced renal hyper proliferation and injury in rats.

机构信息

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

出版信息

Food Chem Toxicol. 2013 Aug;58:530-5. doi: 10.1016/j.fct.2013.04.054. Epub 2013 May 30.

DOI:10.1016/j.fct.2013.04.054
PMID:23727425
Abstract

This study was designed to investigate the effect of butylated hydroxy toluene (BHT), a phenolic antioxidant used in foods, cosmetics and pharmaceutical products, on Fe-NTA-induced nephrotoxicity in rats. Fe-NTA (alone) treatment enhances ornithine decarboxylase activity to 5.3-fold, and [(3)H] thymidine incorporation in DNA to 3.5-fold compared with the corresponding saline treated control. The enhanced ornithine decarboxylase activity and DNA synthesis showed a reduction to 2.12-2.15-fold respectively at a higher dose of 2 mg BHT/day/animal, compared with the Fe-NTA treated group. Fe-NTA treatment also enhanced the renal microsomal lipid peroxidation to 2.0-fold and decreased the activities of glutathione and antioxidant enzymes to a range of 2.2-2.5-fold in kidney. These changes were reversed significantly in animals receiving a pretreatment of BHT. Present data suggests that BHT can prevent the toxic effects of Fe-NTA and can serve as a potent chemopreventive agent to suppress oxidant-induced tissue injury and nephrotoxicity in rats.

摘要

本研究旨在探讨丁基羟基甲苯 (BHT) 对 Fe-NTA 诱导的大鼠肾毒性的影响。BHT 是一种酚类抗氧化剂,用于食品、化妆品和医药产品中。Fe-NTA(单独)处理使鸟氨酸脱羧酶活性增强 5.3 倍,DNA 中 [(3)H] 胸腺嘧啶掺入增加 3.5 倍,与相应的生理盐水处理对照组相比。与 Fe-NTA 处理组相比,高剂量 2mg BHT/天/动物时,增强的鸟氨酸脱羧酶活性和 DNA 合成分别降低至 2.12-2.15 倍。Fe-NTA 处理还使肾微粒体脂质过氧化增强 2 倍,并使肾脏中的谷胱甘肽和抗氧化酶活性降低到 2.2-2.5 倍的范围内。这些变化在接受 BHT 预处理的动物中明显逆转。目前的数据表明,BHT 可以预防 Fe-NTA 的毒性作用,并可以作为一种有效的化学预防剂,抑制氧化剂诱导的组织损伤和大鼠的肾毒性。

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