Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/51805
標題: β-胡蘿蔔素與抗壞血酸之交互作用
The interaction of β-carotene with ascorbic acid
作者: 吳家淑
Wu, Chia-Shu
關鍵字: β-胡蘿蔔素;抗壞血酸;人類上皮成纖母細胞;人類胚胎腸道細胞
出版社: 食品科學系
摘要: 
過去許多流行病學研究顯示膳食中多攝取深色的蔬菜水果可以減低癌症與心血管疾病的發生率。一般認為這是由於這些食物中富含β-carotene之故。但臨床實驗顯示抽煙者補充β-carotene不僅沒有益處,甚至可能增加肺癌的發生率。另外文獻也指出抽煙者的血清中維生素C含量比正常人顯著為低。有假說認為抽煙者體內沒有足夠的維生素C可以還原或阻止β-carotene進一步氧化,因此補充β-carotene反而增加其肺癌發生率。本研究針對此一種假說加以驗證,亦即:人體中的抗氧化成分β-carotene及ascorbic acid可能產生交互作用;ascorbic acid可能藉由直接或間接保護或還原β-carotene而減少β-carotene氧化產物所造成之傷害。本研究採用二個試驗模式:(1)簡單的膜系統,即由phosphatidylcholine所製備的微脂粒(liposome);(2)人類上皮成纖母細胞(Hs68)及人類胚胎腸道細胞(Intestine 407;Int407)兩株細胞。此二模式分別以UVA或2,2’-azobis (2,4-dimethylvaleronitrile) (AMVN)處理,探討當β-carotene處於氧化壓力下:(1)ascorbic acid是否對β-carotene 具有保護或還原其自由基作用;(2)此二者之交互作用是直接或間接發生。
將微脂粒、Hs68細胞及Int407細胞分別與不同型態之ascorbic acid及β-carotene進行預培養,再以UVA或AMVN處理,接著進行氧化傷害及各種抗氧化維生素之分析。結果顯示:(1)微脂粒系統中,AA可顯著降低脂質過氧化,而DHA則無此效果。(2)在細胞模式中適量之AA 及DHA均顯著增加細胞存活率,減少脂質過氧化及DNA傷害。(3)增加微脂粒及細胞中ascorbic acid的含量可以延緩β-carotene的消耗,但β-carotene含量並非在抗壞血酸消耗後才顯著降低,因此AA具有減少β-carotene損耗及促氧化性的效果,但AA直接將β-carotene自由基還原之可能性相當低。上述結果說明:當β-carotene處於氧化壓力下時,ascorbic acid確實對β-carotene具有保護作用,而此作用應是間接性的而非直接還原β-carotene自由基。

Epidmiological studies demonstrate an inverse relationship between the intake of dark vegetables and fruits and the risk of cancers and cardiovascular disease, especially in smokers. The effects have been attributed to β-carotene. However, two clinical trials of supplemental β-carotene produce disappointing results, that is, β-carotene supplemtation is detrimental in smokers. Additionally, the smokers have lower serum levers of vitamin C than do nonsmokers. One of the theories that have been proposed regarding the possible pro-carcinogenic effect in smokers holds that smokers may not have enough vitamin C to recycle or stop the chain reaction of the radical cation of b-carotene, which could damage cellular macromolecules including DNA. Using liposome and two human cell lines, human foreskin fibroblasts (Hs68 cells) and human embryo intestine (Int407 cells), we determined whether ascorbic acid (AA) reduces b-carotene oxidation induced by exposure to UVA or by incubation with 2,2'-azobis (2,4-dimethylvaleronitrile) (AMVN). We also investigated whether such protection involves direct recycling of b-carotene by ascorbic acid.
Liposome and cells were enriched with b-carotene, AA or dehydroascorbate (DHA) for 1 or 24 hr before exposure to UVA or incubation with AMVN. We found that: (1) In liposome, 20mM AA, but not DHA, significantly reduced lipid peroxidation; (2) In cells, 20mM AA and DHA significantly increased the viability of cells and inhibited lipid peroxidation and DNA damage. The protective effects depended on the molar ratio of AA/BC in cells; and (3) AA or DHA only retarded the consumption of b-carotene but not completely spared b-carotene. The results suggest that AA protects b-carotene in liposome or cells by an indirect, rather than direct recycling mechanism.
URI: http://hdl.handle.net/11455/51805
Appears in Collections:食品暨應用生物科技學系

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