Attenuation by boron supplementation of the biochemical changes associated with thioacetamide-induced hepatic lesions

Shakir Ali, G. Diwakar, Sonica Pawa, M.R. Siddiqui, S.K. Jain, M Abdulla
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引用次数: 4

Abstract

Acute hepatic failure is a severe complication induced by certain chemicals, drugs, or virus. Thioacetamide generally has been used for the study of hepatic failure in experimental animal model. The present study was aimed at to examine the role of boron in the pathogenesis of acute hepatic failure in rats. A single intraperitoneal injection of thioacetamide produced severe liver injury, as manifested by elevation in serum aminotransferases, alkaline phosphatase, and hepatic lipid peroxidation. Boron, when administered in the form of boric acid for three consecutive days followed by thioace-tamide, attenuated thioacetamide-mediated changes in the level of these biochemical parameters in a dose-dependent manner. The effect of boron supplementation on the survival rates of rats treated with a lethal dose of thioacetamide was also determined and found to lower the mortality rates in the group of animals supplemented with boron followed by thioacetmide. The effects on biochemical parameters and the survival rates were dependent on the dose of boron administered as boric acid. It is concluded that boron provides protection against the thioacetamide-induced acute hepatic failure in rats in a dose-dependent manner. J. Trace Elem. Exp. Med. 15: 47–55, 2002. © 2002 Wiley-Liss, Inc.
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补硼对硫代乙酰胺肝损伤相关生化变化的影响
急性肝功能衰竭是由某些化学物质、药物或病毒引起的严重并发症。硫代乙酰胺通常用于实验动物模型中肝衰竭的研究。本研究旨在探讨硼在大鼠急性肝功能衰竭发病机制中的作用。单次腹膜内注射硫代乙酰胺会导致严重的肝损伤,表现为血清转氨酶、碱性磷酸酶和肝脏脂质过氧化升高。当硼以硼酸的形式连续给药三天,然后给药硫代乙酰胺时,以剂量依赖的方式减弱了硫代乙酰胺介导的这些生化参数水平的变化。还测定了补充硼对用致死剂量的硫代乙酰胺治疗的大鼠存活率的影响,并发现补充硼后补充硫代乙酰胺的动物组的死亡率较低。对生化参数和存活率的影响取决于以硼酸形式给予的硼的剂量。结论硼对硫代乙酰胺诱导的大鼠急性肝功能衰竭具有剂量依赖性保护作用。J.Trace Elem。Exp.Med.15:47-551002。©2002 Wiley-Liss,股份有限公司。
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International Society For Trace Element Research In Humans (ISTERH) Seventh International Conference, Bangkok, Thailand, November 7–12, 2004 Response† Erratum Fluoride: A toxic or therapeutic agent in the treatment of osteoporosis? Interleukin-1α, tumor necrosis factor-α, and interleukin-12 secreted by zinc-induced murine macrophages in vivo and in vitro
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