Hughes D A, Wright A J, Finglas P M, Peerless A C, Bailey A L, Astley S B, Pinder A C, Southon S
Department of Nutrition, Diet, and Health, Institute of Food Research, Colney, Norwich, UK.
J Lab Clin Med. 1997 Mar;129(3):309-17. doi: 10.1016/s0022-2143(97)90179-7.
Although there is strong epidemiologic evidence that diets rich in carotenoids such as beta-carotene are associated with a reduced incidence of cancer, the cellular mechanisms underlying this phenomenon remain unknown. This article describes the effect of dietary beta-carotene supplementation on both the expression of functionally associated surface molecules on human monocytes and on the secretion of the cytokine tumor necrosis factor-alpha (TNF-alpha) by monocytes, all of which are involved in the initiation and regulation of immune responses involved in tumor surveillance. A double-blind, placebo-controlled, crossover study was undertaken in which 25 healthy, adult male nonsmokers were randomly assigned to receive beta-carotene (15 mg daily) or placebo for 26 days, followed by the alternative treatment for a further 26 days. The expression of functionally related monocyte surface molecules was quantified by flow cytometry, and ex vivo secretion of TNF-alpha was quantified by an enzyme-linked immunosorbent assay, before and after each treatment period. After dietary supplementation there were significant increases in plasma levels of beta-carotene and in the percentages of monocytes expressing the major histocompatibility complex class II molecule HLA-DR and the adhesion molecules intercellular adhesion molecule-1 and leukocyte function-associated antigen-3. In addition, the ex vivo TNF-alpha secretion by blood monocytes was significantly increased after supplementation. These findings suggest that moderate increases in the dietary intake of beta-carotene can enhance cell-mediated immune responses within a relatively short period of time, providing a potential mechanism for the anticarcinogenic properties attributed to beta-carotene.
尽管有强有力的流行病学证据表明，富含类胡萝卜素（如β-胡萝卜素）的饮食与癌症发病率降低有关，但这一现象背后的细胞机制仍不清楚。本文描述了膳食补充β-胡萝卜素对人类单核细胞上功能相关表面分子表达以及单核细胞分泌细胞因子肿瘤坏死因子-α（TNF-α）的影响，所有这些都参与了肿瘤监测中免疫反应的启动和调节。进行了一项双盲、安慰剂对照的交叉研究，25名健康成年男性非吸烟者被随机分配接受β-胡萝卜素（每日15毫克）或安慰剂，为期26天，然后交替治疗26天。在每个治疗期前后，通过流式细胞术对功能相关的单核细胞表面分子表达进行定量，通过酶联免疫吸附测定对TNF-α的体外分泌进行定量。膳食补充后，血浆β-胡萝卜素水平以及表达主要组织相容性复合体II类分子HLA-DR和黏附分子细胞间黏附分子-1和白细胞功能相关抗原-3的单核细胞百分比显著增加。此外，补充后血液单核细胞的体外TNF-α分泌显著增加。这些发现表明，适度增加β-胡萝卜素的膳食摄入量可在相对较短的时间内增强细胞介导的免疫反应，为β-胡萝卜素的抗癌特性提供了一种潜在机制。
