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实验性中耳炎中氧自由基损伤的证据。

Evidence of oxygen radical injury in experimental otitis media.

作者信息

Parks R R, Huang C C, Haddad J

机构信息

Department of Otolaryngology, Columbia Presbyterian Medical Center, New York, N.Y. 10032.

出版信息

Laryngoscope. 1994 Nov;104(11 Pt 1):1389-92. doi: 10.1288/00005537-199411000-00013.

Abstract

Free radicals have been implicated in the pathogenesis of an increasing number of diseases and inflammatory states. They may cause tissue damage by their chemical modification of proteins, carbohydrates, nucleotides, and lipids. Lipid peroxidation occurs as a consequence of free radicals acting on the polyunsaturated fatty acids of cellular membranes. To determine if free radicals play a role in the pathogenesis of otitis media, lipid peroxides and their by-products were assayed in the mucosa of a guinea pig model of otitis media. Both lipid hydroperoxide (LPO) and malondialdehyde (MDA) were measured in the tissues of the middle ear mucosa. Comparisons were made between an infected and a control group. Both LPO and MDA were found to be significantly elevated (P < .01 and P < .05, respectively) in the infected mucosa. Correlation of the biochemical data was made with histologic studies. The significance of these findings as well as suggestions for future experimentation are addressed.

摘要

自由基与越来越多疾病和炎症状态的发病机制有关。它们可能通过对蛋白质、碳水化合物、核苷酸和脂质进行化学修饰而导致组织损伤。脂质过氧化是自由基作用于细胞膜多不饱和脂肪酸的结果。为了确定自由基是否在中耳炎发病机制中起作用,在豚鼠中耳炎模型的黏膜中检测了脂质过氧化物及其副产物。在中耳黏膜组织中测量了脂质过氧化氢(LPO)和丙二醛(MDA)。对感染组和对照组进行了比较。发现在感染的黏膜中LPO和MDA均显著升高(分别为P <.01和P <.05)。将生化数据与组织学研究进行了相关性分析。讨论了这些发现的意义以及对未来实验的建议。

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