摘要
目的通过检测３１３名吸烟者血中自由基水平及α１抗胰蛋白酶（α１ＡＴ）的变化，探讨氧自由基在吸烟致病中的作用。方法试验分为非吸烟组１８９名，轻度吸烟组（１～２９９年支）６８名，中度吸烟组（３００～５９９年支）１８０名；重度吸烟组（＞６００年支）６５名，采用硫代巴比妥酸法、放射免疫法、５′５二硫代安息香酸（ＤＴＮＢ）直接法、Ｅｌｍａｎ法、酶标法分别检测脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨｐｘ），谷胱甘肽（ＧＳＨ）及α１ＡＴ。结果非吸烟者血中ＬＰＯ为４９±２５μｍｏｌ／Ｌ、ＳＯＤ为８７８±３０２ｎｇ／ｇＨｂ、ＧＳＨｐｘ为１２０±３５Ｕ、ＧＳＨ为３４±０７ｍｍｏｌ／Ｌ、α１ＡＴ为７５±１１ｍｇ／Ｌ，吸烟者血中ＬＰＯ为６±３μｍｏｌ／Ｌ、ＳＯＤ为７８０±２８２ｎｇ／ｇＨｂ、ＧＳＨｐｘ为１１２±３４Ｕ、ＧＳＨ为３１±０８ｍｍｏｌ／Ｌ、α１ＡＴ为７１±１５ｍｇ／Ｌ，吸烟者与非吸烟者比较血中ＬＰＯ增高（Ｐ＜０．０１），ＳＯＤ、ＧＳＨｐｘ、ＧＳＨ、α１ＡＴ降低（Ｐ＜０．０５或Ｐ＜０．０１），ＬＰＯ与α１ＡＴ呈负相关（ｒ＝－０．４８９，Ｐ＜０．０１）。结?
Objective Detecting free radicals and α 1 antitrypsin (α 1 AT) from healthy smoker′s blood to study the action of free radicals in smoking induced diseases. Method Thiobarbituric acid method (TBA), RIA, 5 5′ dithio 2 dinitrobenzoicacid (DTNB) method, Ellman method and enzyme linked immunosorbent assay were used to detect the lipid peroxides (LPO), superoxide dismutase (SOD), glutathione peroxidase (GSH px), glutathione (GSH) and α 1 AT. Result In the blood of nonsmokers, LPO was 4.9±2.5 μmol/L、SOD was 878±302 ng/g Hb、GSH px was 120±35 U、GSH was 3.4± 0.7 mmol/L、α 1 AT was 75±11 mg/L,in the blood of smokers, they were 6.1±3.0 μmol/L、780±282 ng/g Hb、112±34 U、3 1±0.8 mmol/L、71±15 mg/L respectively. The LPO content in the blood of smokers was significant higher than that of nonsmokers ( P <0.01), but the SOD GSH px GSH and α 1 AT contents measured was significant lower ( P <0.05 or P <0.01).Conclusion The increase of oxidation and decrease of antioxidation, activity of α 1 AT and inbalance of protease and antiprotease might play important roleg in smoking inducied diseases.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
1998年第4期218-220,共3页
Chinese Journal of Tuberculosis and Respiratory Diseases
