Hulea S A, Olinescu R, Nitã S, Crocnan D, Kummerow F A
University of Illinois, Burnsides Research Laboratory, Urbana 61801, USA.
J Environ Pathol Toxicol Oncol. 1995;14(3-4):173-80.
Cigarette smoking has been shown to be a major risk factor for cardiovascular disease, lung cancer, and respiratory diseases. Due to its high content of oxidants, the cigarette smoke is bound to cause a prooxidant/antioxidant imbalance in the blood plasma and tissues of smokers. The study groups were selected from an apparently healthy population living in urban areas, comprising 200 subjects aged 18 to 80 years, half of whom were smokers. In smokers aged 18 to 45 years, the changes of the plasma prooxidant parameters (i.e., lipid peroxides, leukocyte activation, and the antioxidant ones [thiol concentration, total antioxidant capacity]) were not significantly different from those of the age-matched controls, whereas in the 46 to 80 age group they were. In smokers, both antioxidant erythrocyte enzymes, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), exhibited increased activity in the 18 to 45 age group and decreased activity in the 46 to 80 age group. The differences in enzyme activity between the smoking and nonsmoking groups were highly significant for SOD in all ages, whereas for GSH-Px the difference in activity was significant only in the case of older smokers. These findings would suggest that a process of adaptation takes place in younger smokers, in whom the antioxidant systems are able to counteract the oxidant factors, while in older smokers this process is no longer occurring and the plasma and tissues are under permanent oxidative stress. Our results clearly demonstrated that a prooxidant/antioxidant imbalance exists in the blood of smokers, and the determination of leukocytes stimulation index may be a useful and simple way of assessing the oxidative stress status of these individuals. A hypothesis regarding a possible mechanism linking cigarette smoking to the development of coronary heart disease is presented.
吸烟已被证明是心血管疾病、肺癌和呼吸系统疾病的主要危险因素。由于香烟烟雾中氧化剂含量高，必然会导致吸烟者血浆和组织中的促氧化剂/抗氧化剂失衡。研究组从居住在城市地区的看似健康的人群中选取，包括200名年龄在18至80岁的受试者，其中一半是吸烟者。在18至45岁的吸烟者中，血浆促氧化剂参数（即脂质过氧化物、白细胞活化）和抗氧化剂参数（巯基浓度、总抗氧化能力）的变化与年龄匹配的对照组相比无显著差异，而在46至80岁年龄组中则有差异。在吸烟者中，两种抗氧化红细胞酶，即谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD），在18至45岁年龄组中活性增加，在46至80岁年龄组中活性降低。吸烟组和非吸烟组之间的酶活性差异在所有年龄段的SOD中都非常显著，而对于GSH-Px，只有老年吸烟者的活性差异显著。这些发现表明，年轻吸烟者会发生适应过程，其中抗氧化系统能够抵消氧化因素，而老年吸烟者不再发生这种过程，血浆和组织处于永久性氧化应激状态。我们的结果清楚地表明，吸烟者血液中存在促氧化剂/抗氧化剂失衡，白细胞刺激指数的测定可能是评估这些个体氧化应激状态的一种有用且简单的方法。本文提出了一个关于吸烟与冠心病发展之间可能机制的假设。
