FREE-RADICAL PATHOLOGY IN CHRONIC ARTERIAL-DISEASE
FREE-RADICAL PATHOLOGY IN CHRONIC ARTERIAL-DISEASE
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DOI：
10.1016/0891-5849(89)90082-8
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发表时间：
1989-01-01
影响因子：
7.4
通讯作者：
SMITH, WE
中科院分区：
文献类型：
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作者：
BELCH, JJF;CHOPRA, M;SMITH, WE
有毒氧代谢物的产生通常与炎症有关。然而，病理性自由基反应可通过不利地影响前列环素（PGI2）的合成而引起组织损伤，从而引发凝血。我们通过测量谷胱甘肽浓度（GSH）和超氧化物歧化酶活性（SOD），评估了红细胞对有毒氧代谢物产生的防御变化。测量了20例外周动脉疾病患者、22例血管炎患者和11例心绞痛患者的GSH和SOD，并与17例匹配的对照进行了比较。53例动脉疾病患者的SOD水平明显降低，而GSH水平则明显升高。细胞外血浆硫醇（PSH）水平较低，血浆紫蛋白（Cp）水平较高。我们认为自由基病理不仅存在于炎性血管疾病中，也存在于动脉粥样硬化中。
The generation of toxic oxygen metabolites is more usually associated with inflammation. However, pathological free radical reactions can cause tissue damage by adversely affecting prostacyclin (PGI2) synthesis allowing initiation of coagulation. We have assessed changes in the red cell defence to toxic oxygen metabolite generation, viz measurement of glutathione concentration (GSH) and superoxide dismutase activity (SOD). GSH and SOD were measured in 20 patients with peripheral arterial disease, 22 patients with vasculitis, and 11 patients with angina, and compared to 17 matched controls. The 53 subjects with arterial disease had significantly lower SOD levels: in contrast GSH levels were significantly higher. Extracellularly plasma thiol levels (PSH) were low and caeruloplasmin (Cp) levels were high. We suggest that free radical pathology exists not only inflammatory vascular disease but also in atheroclerosis.