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黄曲霉毒素 B(1)诱导鱼类(罗非鱼)脂质和蛋白质氧化损伤——甘露丸的保护作用。

Oxidative damage to lipids and proteins induced by aflatoxin B(1) in fish (Labeo rohita)-protective role of Amrita Bindu.

机构信息

Department of Medical Biochemistry, Dr. ALM Post Graduate of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.

出版信息

Environ Toxicol Pharmacol. 2004 Jun;17(2):73-7. doi: 10.1016/j.etap.2004.03.002.

DOI:10.1016/j.etap.2004.03.002
PMID:21782716
Abstract

In the present study, fish (Labeo rohita) were treated with a single intraperitoneal administration of aflatoxin B(1) (AFB(1)) (100μg/100gBW). The resultant oxidative damage to lipids (measured as conjugated diene and lipid peroxidation (LPO)) and proteins (protein carbonyl) in liver, kidney and brain at the end of 3rd and 6th day was assessed. Our results showed that AFB(1) induced a significant increase in conjugated diene formation and LPO not only in liver but also in kidney and brain. A parallel increase in protein carbonyl level was observed in these tissues. When 1:1 mixture of 20% solution of Amrita Bindu (a salt-spice-herbal mixture based on Indian system of medicine) was co-administered along with 100μg AFB(1), the AFB(1) induced increase in conjugated diene, LPO and protein carbonylation were minimised to a greater extent. These results led to conclusion that (i) AFB(1) not only induces oxidative damage to the primary target organ-liver in L. rohita, but also in kidney and brain, (ii) co-administration of Amrita Bindu confers protection to lipids and protein against the AFB(1) induced oxidative damage in all the three tissues.

摘要

在本研究中,采用单次腹腔注射黄曲霉毒素 B1(AFB1)(100μg/100gBW)的方法处理鱼类(Labeo rohita)。在第 3 天和第 6 天结束时,评估肝脏、肾脏和大脑中脂质(以共轭二烯和脂质过氧化(LPO)衡量)和蛋白质(蛋白质羰基)的氧化损伤。我们的结果表明,AFB1 不仅在肝脏中,而且在肾脏和大脑中均诱导共轭二烯形成和 LPO 的显著增加。在这些组织中观察到蛋白质羰基水平的平行增加。当用 100μg AFB1 一起给予印度草药混合物 Amrita Bindu(基于印度医学系统的盐香料草药混合物)的 20%溶液的 1:1 混合物时,AFB1 诱导的共轭二烯、LPO 和蛋白质羰基化的增加被极大地最小化。这些结果得出结论:(i)AFB1 不仅在 L. rohita 的主要靶器官肝脏中诱导氧化损伤,而且在肾脏和大脑中也诱导氧化损伤,(ii)Amrita Bindu 的共同给药在所有三种组织中都能防止脂质和蛋白质受到 AFB1 诱导的氧化损伤。

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