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首页> 外文期刊>Archives of Toxicology >Exposure to acetaminophen impairs vasodilation, increases oxidative stress and changes arterial morphology of rats
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Exposure to acetaminophen impairs vasodilation, increases oxidative stress and changes arterial morphology of rats

机译：暴露于乙酰氨基酚损害血管舒张，增加氧化应激并改变大鼠的动脉形态

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Acetaminophen (APAP) is one of the most widely consumed drugs in the world. Studies have shown renal and hepatic damage as the direct result of high oxidative stress induced by APAP. Since the cardiovascular system is sensitive to oxidative stress and literature describes increased cardiovascular dysfunction in APAP consumers, this work aimed to evaluate harmful effects of APAP on the vascular system. Rats were exposed to APAP (400mg/kg/day in drinking water) for 14days. Plasma and aortas were collected and stored in -80 degrees C and a selection of arteries was prepared for isometric tension recordings, morphological, immunohistochemical and protein expression analysis. The APAP-treated group presented increased transaminases (ALT/AST) and malondialdehyde levels in the plasma compared to controls. Lipid peroxidation, glutathione reductase and superoxide dismutase levels were increased in the plasma and arteries of the APAP group. Nevertheless, glutathione level was reduced as compared to control group. The vasodilation response to acetylcholine and sodium nitroprusside (0.1nM to 10 mu M) was also impaired after APAP treatment; however, the vascular relaxation was restored after treatment with vitamin C (100 mu M). Arteries from the APAP group presented reduced wall thickness, collagen deposition, elastic fibers and increased immunoreactivity to nitrotyrosine. eNOS and sGC protein expression remained unchanged and were at similar levels as controls. These findings showed higher oxidative stress and impaired vasodilation in rats exposed to APAP. Furthermore, arteries presented reduced cell layers, collagen, elastin deposition and significantly increased immunoreactivity to nitrotyrosine after APAP treatment.
机译：乙酰氨基酚（APAP）是世界上最广泛消耗的药物之一。研究表明，肾和肝损伤是通过APAP诱导的高氧化应激的直接结果。由于心血管系统对氧化应激和文献敏感，因此APAP消费者中的心血管功能障碍增加，这项工作旨在评估APAP对血管系统的有害影响。将大鼠暴露于14天的APAP（饮用水400mg / kg /天）。收集血浆和主动脉并储存在-80℃，为等距张力记录，形态，免疫组织化学和蛋白质表达分析制备了一系列动脉。与对照相比，APAP处理基团呈现血浆中的转氨酶（ALT / AST）和丙二醛水平。在APAP组的血浆和动脉中增加了脂质过氧化，谷胱甘肽还原酶和超氧化物歧化酶水平。然而，与对照组相比，谷胱甘肽水平降低。在APAP处理后，还损害对乙酰胆碱和亚硝酸钠（0.1nm至10μm）的血管舒张响应;然而，用维生素C（100μm）处理后血管弛豫恢复。 APAP组的动脉呈现壁厚减少，胶原沉积，弹性纤维和对硝基吡肽的增加的免疫反应性。 eNOS和SGC蛋白表达保持不变，并且与对照相似。这些发现显示出更高的氧化应激和暴露于APAP的大鼠的血管舒张。此外，动脉呈现降低的细胞层，胶原蛋白，弹性蛋白沉积，并在APAP处理后显着增加对硝基霉菌的免疫反应性。

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