Miró O, Alonso J R, Casademont J, Jarreta D, Urbano-Márquez A, Cardellach F
Department of Internal Medicine, Hospital Clínic, August Pi i Sunyer, University of Barcelona, Catalonia, Spain.
Toxicol Lett. 1999 Nov 22;110(3):219-23. doi: 10.1016/s0378-4274(99)00161-7.
Increased oxidative damage seems to be a relevant mechanism in the pathophysiology of patients with an acute carbon monoxide (CO) poisoning. We have investigated the degree of membrane oxidative damage through the assessment of lipid peroxidation in circulating lymphocytes from five patients acutely intoxicated by CO. Since mitochondria are a major source of reactive oxygen species and mitochondrial cytochrome c oxidase (COX) has been reported to be inhibited after acute CO poisoning, we have also assessed the lymphocyte COX activity and its relationship with the degree of lipid peroxidation. Data were compared with those from 32 non-smoker healthy controls comparable in terms of age, gender and physical activity. In intoxicated patients, we have found a significant increase of lipid peroxidation compared to control individuals (P < 0.05), as well as a marked COX inhibition (P < 0.001). Both parameters showed a positive, nearly significant correlation (r = 0.81, P = 0.09). We conclude that oxidative damage of lymphocyte membranes is increased after acute CO poisoning, and suggest that such increase could be partially mediated by mitochondrial COX inhibition caused by CO.
氧化损伤增加似乎是急性一氧化碳(CO)中毒患者病理生理学中的一个相关机制。我们通过评估5例急性CO中毒患者循环淋巴细胞中的脂质过氧化作用,研究了膜氧化损伤的程度。由于线粒体是活性氧的主要来源,且据报道急性CO中毒后线粒体细胞色素c氧化酶(COX)会受到抑制,我们还评估了淋巴细胞COX活性及其与脂质过氧化程度的关系。将数据与32名在年龄、性别和身体活动方面相当的非吸烟健康对照者的数据进行了比较。在中毒患者中,我们发现与对照个体相比,脂质过氧化作用显著增加(P < 0.05),同时COX受到明显抑制(P < 0.001)。这两个参数显示出正相关,接近显著相关(r = 0.81,P = 0.09)。我们得出结论,急性CO中毒后淋巴细胞膜的氧化损伤增加,并表明这种增加可能部分由CO引起的线粒体COX抑制介导。