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亚硫酸盐对正常和亚硫酸盐氧化酶缺乏的大鼠红细胞抗氧化酶和脂质过氧化的影响。

Effect of sulfite on antioxidant enzymes and lipid peroxidation in normal and sulfite oxidase-deficient rat erythrocytes.

机构信息

Faculty of Medicine, Department of Biochemistry, Mustafa Kemal University, Hatay, Turkey.

出版信息

J Physiol Biochem. 2010 Sep;66(3):205-12. doi: 10.1007/s13105-010-0025-7. Epub 2010 Jun 23.

Abstract

Sulfite and related chemical such as sulfite salts and sulfur dioxide has been used as a preservative in food and drugs. This molecule has also been generated from the catabolism of sulfur-containing amino acids. Sulfite is a very reactive and potentially toxic molecule and has to be detoxified by the enzyme sulfite oxidase (SOX). The aim of this study was to investigate the effects of ingested sulfite on erythrocyte antioxidant status by measuring glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and oxidant status by measuring thiobarbituric acid reactive substances (TBARS) in normal and SOX-deficient rats. Rats were assigned to four groups (n = 10 rats/group) as follows; control (C), sulfite (CS), deficient (D), and deficient + sulfite (DS). SOX deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25 mg/kg) was administered to the animals via their drinking water. At the end of 6 weeks, Erythrocyte G-6-PD, SOD, and GPx but not CAT activities were found to be significantly increased with and without sulfite treatment in SOX-deficient groups. Sulfite treatment alone was also significantly increased erythrocytes' SOD activity in CS group compared to control. TBARS levels were found to be significantly increased in CS and DS groups and decreased in D group. When SOX-deficient rats treated with sulfite, TBARS level was still higher than other groups. In conclusion, these results suggested that erythrocyte antioxidant capacity, a defense mechanism against the oxidative challenge, increased by endogenous and exogenous sulfite due to its oxidant nature. This increase was also observed in CS and DS groups but it was insufficient to prevent lipid peroxidation.

摘要

亚硫酸盐和相关化学物质(如亚硫酸盐盐和二氧化硫)已被用作食品和药物中的防腐剂。这种分子也可以从含硫氨基酸的分解代谢中产生。亚硫酸盐是一种非常活跃且潜在有毒的分子,必须通过亚硫酸盐氧化酶(SOX)进行解毒。本研究旨在通过测量葡萄糖-6-磷酸脱氢酶(G-6-PD)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性以及通过测量硫代巴比妥酸反应物质(TBARS)来研究摄入亚硫酸盐对红细胞抗氧化状态的影响。在正常和 SOX 缺乏的大鼠中。将大鼠分为四组(每组 10 只大鼠);对照组(C)、亚硫酸盐(CS)、缺乏组(D)和缺乏+亚硫酸盐(DS)。SOX 缺乏症通过喂养大鼠低钼饮食并在饮用水中添加 200ppm 钨(W)来建立。亚硫酸盐(25mg/kg)通过饮用水给予动物。在 6 周结束时,发现 SOX 缺乏组中 G-6-PD、SOD 和 GPx 的红细胞活性,但 CAT 活性没有明显增加,无论是否用亚硫酸盐处理。亚硫酸盐处理也显著增加了 CS 组中红细胞的 SOD 活性,与对照组相比。CS 和 DS 组的 TBARS 水平明显升高,D 组降低。当 SOX 缺乏的大鼠用亚硫酸盐处理时,TBARS 水平仍高于其他组。总之,这些结果表明,由于其氧化性质,内源性和外源性亚硫酸盐增加了红细胞的抗氧化能力,这是一种抵抗氧化挑战的防御机制。这种增加在 CS 和 DS 组中也观察到,但不足以防止脂质过氧化。

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