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β-胡萝卜素对大鼠DNA氧化及烷化损伤影响的研究
引用本文:梁惠,韩磊,马爱国.β-胡萝卜素对大鼠DNA氧化及烷化损伤影响的研究[J].卫生研究,2005,34(3):316-318.
作者姓名:梁惠  韩磊  马爱国
作者单位:1. 青岛大学医学院医学营养研究所,青岛,266021
2. 青岛大学医学院附属医院
基金项目:国家自然科学基金资助项目 (No .30 0 70 659)
摘    要:目的 研究β-胡萝卜素(β- C)对大鼠DNA氧化及烷化损伤的影响,初步探讨其抗氧化作用机制。方法 将大鼠随机分为5组,分别为β- C缺乏组(β-C1组)、补充0 . 0 71mg (kg·d) (βC2组)、0 . 35 5mg (kg·d) (βC3组)、4 . 2 8mg (kg·d) (βC4组)、15 . 0mg (kg·d) (βC5组)。微量荧光法测大鼠血浆中VA含量;单细胞凝胶电泳(SCGE)观察淋巴细胞DNA氧化损伤状况;高效毛细管电泳法测尿中O6 甲基鸟嘌呤(O6 MeG)的排出量。结果 经8周干预后,四个βC补充组血浆中VA的水平为2 76~30 6 μg L ,缺乏组血浆中VA的含量为135 μg L ,明显低于补充组(P <0 . 0 1)。DNA损伤结果显示:缺乏组大鼠淋巴细胞DNA自发性损伤明显高于补充组(P <0 . 0 1)。H2 O2 诱导的淋巴细胞氧化损伤,4 .2 8mg (kg·d)组淋巴细胞氧化损伤明显低于其他4个组(P <0 . 0 1)。β- C各补充剂量组的O6 MeG的排出量在第6周和第8周时均明显低于缺乏组(P <0 . 0 5 )。O6 MeG排出量并未随着补充剂量的增加而减少,4 .2 8mg (kg·d)组尿中O6 MeG排出量在第8周时最低。结论 β- C较长时间缺乏可导致DNA自发损伤、H2 O2 诱导的氧化损伤以及烷化损伤均明显增加;大剂量β-C15 . 0mg (kg·d)补充对DNA损伤无明显防护作用,适量摄入β- C 4 . 2 8mg (kg·

关 键 词:β-胡萝卜素  单细胞凝胶电泳  抗氧化  DNA损伤  O6-甲基鸟嘌呤
文章编号:1000-8020(2005)03-0316-03
修稿时间:2004年7月13日

Effect of β-carotene supplementation on DNA oxidative and alkylation damage in rats
Liang Hui,Han Lei,MA Ai-guo.Effect of β-carotene supplementation on DNA oxidative and alkylation damage in rats[J].Journal of Hygiene Research,2005,34(3):316-318.
Authors:Liang Hui  Han Lei  MA Ai-guo
Institution:Institute of Human Nutrition Medical, College of Qingdao University, Qingdao 266021, China.
Abstract:OBJECTIVE: To investigate the effect of beta-carotene (P-C) supplementation on DNA oxidative and alkylation damage in rats. METHODS: Rats were randomly divided into five groups. The first group was no beta-C, and the second, the third, the forth and the fifth groups were daily supplemented with 0.071, 0.355, 4.28 and 15.0 mg/(kg x d). The content of plasma VA was analyzed by fluorescent spectrometry. DNA damage and oxidative damage induced by H2O2 were detected by single-cell gel electrophoresis (SCGE) and O6-Methyl-guanine (O6-MeG) was measured by high performance capillary zone electrophoresis. RESULTS: After 8 weeks trial, the results showed that levels of plasma retinol converted from beta-C decreased by 135 microg/L in the beta-C deficiency group, which were much lower than 276 - 306 microg/L in other four beta-C supplement groups (P < 0.01). Intrinsic damage of DNA was more severe in the group of beta-C deficiency than the groups supplemented with beta-C (P < 0.01). The lower DNA oxidative damage of lymphocyte, which was induced by H2O2, was found in 4.28 mg/(kg x d) group than deficiency and other supplement groups (P < 0.05). O6-Methyl-guanine of the supplement groups was lower than the beta-C deficient group at the 6th week and 8th week (P < 0.05). O6-Methyl-guanine did not decreasing with the dose increasing and the lowest in the 4.28mg/(kg x d) group. CONCLUSION: Beta-C or retinol deficiency and over intake such as 15.0 mg/(kg x d) as well might cause or promote DNA damage, and a moderate amount such as 4.280 mg/(kg x d) could improve antioxidative and decrease DNA damage effectively.
Keywords:carotene  SCGE  DNA damage  O6-Methyl-guanine  antioxidation
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