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首页> 外文期刊>Molecular and Cellular Biochemistry >The effects of acute acetaminophen toxicity on hepatic mRNA expression of SOD, CAT, GSH-Px, and levels of peroxynitrite, nitric oxide, reduced glutathione, and malondialdehyde in rabbit
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The effects of acute acetaminophen toxicity on hepatic mRNA expression of SOD, CAT, GSH-Px, and levels of peroxynitrite, nitric oxide, reduced glutathione, and malondialdehyde in rabbit

机译：对乙酰氨基酚急性毒性对家兔肝脏SOD，CAT，GSH-Px mRNA表达，过氧亚硝酸盐，一氧化氮，还原型谷胱甘肽和丙二醛水平的影响

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摘要

We investigated the regulation of antioxidant system under acetaminophen (AAP) toxicity. Twelve male New Zealand rabbits were divided into two groups with the following treatments: Group 1 animals were intraperitoneally injected with single saline (control). Group 2 animals were treated with intraperitoneal injection of AAP at a dose of 250 mg/kg body weight. Four hours following the treatments, blood samples were collected and the rabbits were sacrificed to collect liver samples. Hepatocellular damage was evaluated by aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels as well as histopathological examinations and immunohistochemical analysis. Tissue-reduced glutathione (GSH), nitric oxide (NO·), and malondialdehyde (MDA) levels were also measured. mRNA expression levels of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) were measured by semi-quantitative RT-PCR. It was found that liver GSH was reduced significantly in AAP-treated rabbits (P < 0.05), while MDA and NO· levels were increased when they were compared to control (P < 0.05). Blood AST and ALT levels were also increased following AAP treatment (P < 0.05). Hepatocellular degeneration and severe necrosis were detected in histopathological examinations. Increased immunostaining was observed for inducible nitric oxide synthase (iNOS) and nitrotyrosine in the liver. There were no changes in mRNA expression levels of SOD, CAT, and GSH-Px after AAP treatment compared to control group. These results suggest that the expression of these enzymes, which are involved in the antioxidant system, may not be altered after AAP toxicity, although classical toxic changes such as depletion of GSH, hepatocellular necrosis, and increased immunostaining for iNOS and nitrotyrosine were detected.
机译：我们研究了对乙酰氨基酚（AAP）毒性下抗氧化剂系统的调节。将十二只雄性新西兰兔分为以下两组，分别进行以下处理：将第1组动物腹膜内注射单一生理盐水（对照组）。第2组动物用腹膜内注射AAP以250mg / kg体重的剂量治疗。治疗后四个小时，收集血液样本，处死兔子以收集肝脏样本。通过天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）的水平以及组织病理学检查和免疫组化分析来评估肝细胞损伤。还测量了组织还原型谷胱甘肽（GSH），一氧化氮（NO ·）和丙二醛（MDA）的水平。通过半定量RT-PCR测量抗氧化酶超氧化物歧化酶（SOD），过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GSH-Px）的mRNA表达水平。研究发现，与对照组相比，AAP处理的兔子的肝脏GSH显着降低（P <0.05），而MDA和NO ·的水平却升高了（P <0.05）。 AAP治疗后血AST和ALT水平也升高（P <0.05）。在组织病理学检查中发现肝细胞变性和严重坏死。肝脏中的诱导型一氧化氮合酶（iNOS）和硝基酪氨酸的免疫染色增加。与对照组相比，AAP治疗后SOD，CAT和GSH-Px的mRNA表达水平没有变化。这些结果表明，尽管检测到经典的毒性变化（例如GSH耗竭，肝细胞坏死以及iNOS和硝基酪氨酸的免疫染色增加），但抗氧化系统中涉及的这些酶的表达可能不会发生改变，尽管AAP毒性已经发生。

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