Phagocyte-produced free radicals: roles in cytotoxicity and inflammation.
Phagocyte-produced free radicals: roles in cytotoxicity and inflammation.
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吞噬细胞产生的自由基：在细胞毒性和炎症中的作用。
DOI：
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
Kenneth Wong
中科院分区：
文献类型：
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作者：
Joe M. McCord;Kenneth Wong
代谢活化的吞噬细胞产生超氧自由基O2-，导致吞噬细胞损伤，表现为体外细胞的过早死亡。细胞毒性剂似乎是通过超氧化物与过氧化氢的反应形成的，并且被认为是羟基自由基或其二级自由基。在体内，两种诱导炎症的动物模型似乎也在很大程度上依赖于吞噬细胞产生的超氧化物，以发展表现为水肿的组织损伤。静脉注射超氧化物歧化酶在这些模型中显示出抗炎活性，但只有当衍生化后才能在循环中保留更长的时间。另一方面，过氧化氢酶或过氧化氢酶衍生物在体内不显示抗炎活性。
The production of superoxide free radical, O2-, by metabolically activated phagocytes results in damage to the phagocyte which is manifested by the premature death of the cell in vitro. The cytotoxic agent appears to be formed by the reaction of superoxide with hydrogen peroxide, and is thought to be hydroxyl radical or a secondary radical thereof. In vivo two animal models of induced inflammation also appear to be largely dependent on superoxide production by phagocytes for the development of tissue damage manifested as oedema. Intravenously administered superoxide dismutase shows anti-inflammatory activity in these models, but only when so derivatized that it can remain in the circulation for longer periods of time. Catalase, or a catalase derivative, on the other hand, shows no anti-inflammatory activity in vivo.