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粒细胞和巨噬细胞产生毒性氧自由基的机制及其在炎症过程中的作用。

Mechanism of production of toxic oxygen radicals by granulocytes and macrophages and their function in the inflammatory process.

作者信息

Rossi F, Bellavite P, Berton G, Grzeskowiak M, Papini E

出版信息

Pathol Res Pract. 1985 Aug;180(2):136-42. doi: 10.1016/S0344-0338(85)80161-8.

Abstract

The paper deals with 1) the features of the respiratory burst (increase of the respiration with production of O2 metabolites, O2-, H2O2, OH) of the inflammatory cells; 2) the factors responsible for its activation; 3) the methods for its measurement; 4) the molecular events which take place at the level of the plasma membrane following the interaction between the stimuli and the cell surface (the Ca++ changes, the modification of membrane potential, the activation of phospholipid turnover) and the hypothesis of the activation of the protein kinase C; 5) the nature of the NADPH oxidase whose activation is responsible for the respiratory burst and the production of O2 metabolites; 6) the defensive, toxic, proinflammatory and modulatory effects due to the reactivity of the oxygen metabolites.

摘要

本文探讨了

1)炎症细胞呼吸爆发的特征(呼吸增强并产生O2代谢产物O2-、H2O2、OH);2)其激活的相关因素;3)测量方法;4)刺激与细胞表面相互作用后在质膜水平发生的分子事件(Ca++变化、膜电位改变、磷脂代谢激活)以及蛋白激酶C激活的假说;5)负责呼吸爆发和O2代谢产物产生的NADPH氧化酶的性质;6)氧代谢产物反应性所产生的防御、毒性、促炎和调节作用。

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