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聚甲基丙烯酸甲酯热降解产物的毒性

Toxicity of polymethylmethacrylate thermodegradation products.

作者信息

Vainiotalo S, Zitting A, Jacobsson S, Nickels J, Koskinen H, Savolainen H

出版信息

Arch Toxicol. 1984 Jul;55(2):137-42. doi: 10.1007/BF00346053.

Abstract

Polymethylmethacrylate was thermally degraded in air at 300 degrees C and the volatile decomposition products studied with gas chromatography-mass spectrometry. The main product was monomeric methacrylate, although many other compounds existed among the products. Electron spin resonance spectroscopy revealed the presence of free radicals. Wistar rats were exposed to the fumes of the plastic (300 degrees C) and their lungs and brain studied for biochemical effects. In the lung, the activity of 7-ethoxycoumarin O-deethylase decreased and an initial inhibition of glutathione peroxidase and superoxide dismutase was observed. The contents of reduced nonprotein sulfhydryl groups were decreased in the lung and brain. The exposures enhanced the activities of acetylcholine esterase, creatine kinase and NADPH-diaphorase in the brain. Scanning electron microscopy of the exposed lungs showed disorganization of ciliated cells, and the epithelial serous cells (Clara cells) were damaged.

摘要

聚甲基丙烯酸甲酯在300摄氏度的空气中进行热降解,并采用气相色谱-质谱联用技术研究挥发性分解产物。主要产物是甲基丙烯酸单体,尽管产物中还存在许多其他化合物。电子自旋共振光谱显示存在自由基。将Wistar大鼠暴露于该塑料(300摄氏度)的烟雾中,并研究其肺和脑的生化效应。在肺中,7-乙氧基香豆素O-脱乙基酶的活性降低,并且观察到谷胱甘肽过氧化物酶和超氧化物歧化酶最初受到抑制。肺和脑中还原型非蛋白巯基的含量降低。暴露增强了脑中乙酰胆碱酯酶、肌酸激酶和NADPH-黄递酶的活性。对暴露后的肺进行扫描电子显微镜检查显示纤毛细胞紊乱,上皮浆液细胞(克拉拉细胞)受损。

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