Polidori M Cristina, Mecocci Patrizia, Stahl Wilhelm, Sies Helmut
Institute of Biochemistry and Molecular Biology I, Heinrich-Heine University, PO Box 101007, , D-40001 Düsseldorf, Germany.
Br J Nutr. 2003 Jul;90(1):147-50. doi: 10.1079/bjn2003890.
Cigarette smoking is associated epidemiologically with increased risk of cardiovascular diseases, but the pathophysiological mechanisms are still not fully understood. There is evidence that smoking is related to increased free radical production and antioxidant depletion, but the effects of smoking cessation on plasma concentrations of antioxidants and susceptibility to oxidative stress are largely unknown. Plasma levels of vitamins A, C, E, uric acid, total thiols, carotenoids (including lutein, zeaxanthin, beta-cryptoxanthin, lycopene, alpha- and beta-carotene) and malondialdehyde (MDA, a biomarker of lipid peroxidation) were measured in fifteen healthy, normolipidaemic subjects (seven males, eight females, 35.2 (sd 2.3) years) before and 4 weeks after smoking cessation. To determine plasma resistance towards oxidative challenge, plasma was incubated for up to 5 h with the peroxyl radical-generator 2,2'-azobis(2-amidinopropane) (AAPH); MDA and ascorbate levels were measured at various time points. The concentrations of all plasma antioxidants were lower before smoking cessation than afterwards; MDA levels were higher before than after termination of smoking. Upon AAPH exposure, the consumption of plasma ascorbate and the production of MDA occurred at a significantly faster rate before smoking cessation as compared with afterwards. Cigarette smoking cessation is followed by a marked increase in plasma antioxidant concentrations and substantially improves plasma resistance towards oxidative challenge. Given the importance of cigarette smoking as a risk factor for cardiovascular diseases and the pathophysiological role played by oxidative stress in these illnesses, quitting smoking represents an irreplaceable preventive strategy against tobacco-induced oxidative stress and vascular damage.
从流行病学角度来看，吸烟与心血管疾病风险增加有关，但病理生理机制仍未完全明确。有证据表明，吸烟与自由基产生增加和抗氧化剂消耗有关，但戒烟对血浆抗氧化剂浓度和氧化应激易感性的影响在很大程度上尚不清楚。在15名健康、血脂正常的受试者（7名男性，8名女性，年龄35.2（标准差2.3）岁）戒烟前和戒烟4周后，测量了血浆中维生素A、C、E、尿酸、总硫醇、类胡萝卜素（包括叶黄素、玉米黄质、β-隐黄质、番茄红素、α-和β-胡萝卜素）和丙二醛（MDA，脂质过氧化的生物标志物）的水平。为了确定血浆对氧化应激的抵抗力，将血浆与过氧自由基发生器2,2'-偶氮二异丁脒盐酸盐（AAPH）孵育长达5小时；在不同时间点测量MDA和抗坏血酸水平。所有血浆抗氧化剂的浓度在戒烟前低于戒烟后；MDA水平在戒烟前高于戒烟后。与戒烟后相比，暴露于AAPH时，血浆抗坏血酸的消耗和MDA的产生在戒烟前的速率明显更快。戒烟后，血浆抗氧化剂浓度显著增加，并显著提高了血浆对氧化应激的抵抗力。鉴于吸烟作为心血管疾病危险因素的重要性以及氧化应激在这些疾病中所起的病理生理作用，戒烟是预防烟草诱导的氧化应激和血管损伤的不可替代的策略。
