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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >N-acetylcysteine (NAC) diminishes the severity of PCB 126-induced fatty liver in male rodents
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N-acetylcysteine (NAC) diminishes the severity of PCB 126-induced fatty liver in male rodents

机译：N-乙酰半胱氨酸（NAC）减少了雄性啮齿动物中PCB 126诱导的脂肪肝的严重程度

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摘要

Potent aryl hydrocarbon receptor agonists like PCB 126 (3,3',4,4',5-pentachlorobiphenyl) cause oxidative stress and liver pathology, including fatty liver. Our question was whether dietary supplementation with N-acetylcysteine (NAC), an antioxidant, can prevent these adverse changes. Male Sprague-Dawley rats were fed a standard AIN-93G diet (sufficient in cysteine) or a modified diet supplemented with 1.0% NAC. After one week, rats on each diet were exposed to 0, 1, or 5. μmol/kg body weight PCB 126 by i.p. injection (6 rats per group) and euthanized two weeks later. PCB-treatment caused a dose-dependent reduction in growth, feed consumption, relative thymus weight, total glutathione and glutathione disulfide (GSSG), while relative liver weight, glutathione transferase activity and hepatic lipid content were dose-dependently increased with PCB dose. Histologic examination of liver tissue showed PCB 126-induced hepatocellular steatosis with dose dependent increase in lipid deposition and distribution. Dietary NAC resulted in a reduction in hepatocellular lipid in both PCB groups. This effect was confirmed by gravimetric analysis of extracted lipids. Expression of CD36, a scavenger receptor involved in regulating hepatic fatty acid uptake, was reduced with high dose PCB treatment but unaltered in PCB-treated rats on NAC-supplemented diet. These results demonstrate that NAC has a protective effect against hepatic lipid accumulation in rats exposed to PCB 126. The mechanism of this protective effect appears to be independent of NAC as a source of cysteine/precursor of glutathione.
机译：强大的芳基烃受体激动剂，如PCB 126（3,3'，4,4'，5-五氯联苯）会引起氧化应激和肝脏疾病，包括脂肪肝。我们的问题是，饮食中添加抗氧化剂N-乙酰半胱氨酸（NAC）是否可以预防这些不良变化。给雄性Sprague-Dawley大鼠喂食标准AIN-93G饮食（半胱氨酸充足）或补充1.0％NAC的改良饮食。一周后，每只大鼠的i.p.暴露于0、1或5。μmol/ kg体重的PCB 126。注射（每组6只大鼠）并在两周后安乐死。 PCB处理导致生长，饲料消耗，相对胸腺重量，总谷胱甘肽和谷胱甘肽二硫化物（GSSG）的剂量依赖性降低，而相对肝脏重量，谷胱甘肽转移酶活性和肝脂质含量随PCB剂量呈剂量依赖性增加。肝组织的组织学检查显示，PCB 126诱导的肝细胞脂肪变性与脂质沉积和分布的剂量依赖性增加有关。饮食NAC导致两个PCB组的肝细胞脂质减少。通过提取的脂质的重量分析证实了该效果。高剂量PCB处理可降低CD36（一种参与调节肝脂肪酸摄取的清除剂受体）的表达，但在补充NAC饮食的PCB处理大鼠中其表达未改变。这些结果表明，NAC对暴露于PCB 126的大鼠肝脂质具有保护作用。这种保护作用的机制似乎独立于NAC作为半胱氨酸/谷胱甘肽的前体来源。

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