摘要
目的 研究 β 胡萝卜素对香烟烟气诱导脂质过氧化的交互作用。 方法 建立了大鼠肺Ⅱ型细胞体外培养模型 ,加入 β 胡萝卜素或 和香烟烟气颗粒提取物染毒 2 4h后 ,检测细胞的丙二醛 (MDA)含量。并构建短期动物模型 ,使小鼠暴露于香烟烟气和 或补充 β 胡萝卜素 10天 ,检测血清MDA的含量。结果 在大鼠肺Ⅱ型细胞模型中 ,随香烟烟气颗粒提取物的含量增加 ,MDA水平明显上升 ,而 β 胡萝卜素各剂量组间MDA水平的差异无显著性。0 5 μg ml的 β 胡萝卜素可抑制香烟烟气颗粒提取物对肺细胞脂质过氧化的诱导作用 ,表现为拮抗作用。在小鼠动物模型中 ,烟气暴露组的MDA水平显著高于正常对照组 ,而 β 胡萝卜素各剂量组间MDA水平的差异无显著性。给予 β 胡萝卜素 2 5mg kgBW的烟气暴露组小鼠血清中MDA水平下降。结论 β 胡萝卜素对香烟烟气诱导的脂质过氧化具有拮抗作用 ,其有效作用剂量在大鼠肺Ⅱ型细胞实验中为 0 5 μg ml ,在小鼠实验中为 2 5mg kgBW。
Objective To study the interaction of β carotene on lipid peroxidation induced by the smoke of cigarette. Methods Rat type Ⅱ pneumocytes were isolated, cultured and then exposed to particles extracted from cigarette smoke and/or β carotene for 24h. Malondialdehyde (MDA) in the cells was measured by TBA method. On the other hand, serum MDA of mice given β carotene supplements and/or exposed to cigarette smoke for 10 days was measured. Results\ The particles extracted from cigarette smoke increased the content of MDA in the rat type Ⅱ pneumocytes, and the lipid peroxidation was antagonized by adding 0 5μg/ml of β carotene to the cells simultaneously. The results from the in vivo study showed that serum MDA levels were increased in the cigarette smoke treated groups, and the lipid peroxidation was reduced by treating mice with 2 5mg per kg body weight of β carotene. Conclusion\ β carotene had an antagonistic effect on lipid peroxidation induced by cigarette smoke. The effective dosage of β carotene was 0 5μg/ml for rat pneumocytes and 2 5mg/kg BW weight for mice.
出处
《卫生研究》
CAS
CSCD
北大核心
2004年第2期144-146,F004,共4页
Journal of Hygiene Research
基金
国家自然科学基金资助项目 (No .39980 0 35 )