Effect of beta-carotene supplementation on indices of colonic cell proliferation.

Effect of beta-carotene supplementation on indices of colonic cell proliferation.
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补充β-胡萝卜素对结肠细胞增殖指数的影响。

DOI:
10.1093/jnci/87.23.1781
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发表时间:
1995
期刊:
Journal of the National Cancer Institute
影响因子:
--
通讯作者:
Liao,Y
Liao,Y
中科院分区:
--
文献类型:
--
作者:
Frommel,TO;Mobarhan,S;Doria,M;Halline,AG;Luk,GD;Bowen,PE;Candel,A;Liao,Y

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背景:流行病学研究表明,食用含有β-胡萝卜素的食物与结肠癌发病率降低有关。这种联系的有效性最近受到质疑。目前尚不清楚有无结肠息肉或癌症病史的个体之间结肠细胞增殖的速率是否不同,以及增殖是否响应于β-胡萝卜素而变化。目的:本研究旨在(a)确定有无结肠息肉或肿瘤病史的个体中结肠细胞增殖是否存在差异,(B)证明饮食补充后β-胡萝卜素在结肠粘膜中积累,以及(c)确定粘膜β-胡萝卜素积累是否影响结肠细胞增殖。受试者从1991年6月至1994年2月入组I期研究。参与者包括20人(11名男性和9名女性,年龄62.3 ± 8.9岁[平均值± SD]),结肠正常(根据最近的结肠镜检查判断),40(男24例,女16例,年龄59.6 ± 10.1岁),有结肠息肉病史,(30例男性和11例女性,年龄67.2 ± 9.7岁),既往患有结肠癌。后两组受试者每天早晨摄入30 mg β-胡萝卜素或安慰剂,持续3个月。这种剂量的β-胡萝卜素没有已知的毒性作用,但它可以使血清水平增加约10倍。在补充β-胡萝卜素或安慰剂之前和之后收集的样品中,通过高压液相色谱法定量血清和结肠组织中的β-胡萝卜素浓度。根据组织鸟氨酸脱羧酶活性、尿多胺排泄和增殖细胞核抗原表达评估细胞增殖。分别通过Wilcoxon配对符号秩和检验和Mann-Whitney检验评价了不同组内和不同组间由于β-胡萝卜素补充引起的结肠细胞增殖参数的差异。结果:结肠细胞增殖在患有和不患有结肠息肉或癌症的个体中没有差异,血清和结肠组织中β-胡萝卜素浓度在接受β-胡萝卜素的组中显著增加(P<0.001)。然而,细胞增殖并没有不同,判断的任何三个措施,从所有实验组之间收集的样本之前和之后补充β-carotene.Conclusions:膳食补充β-胡萝卜素为期3个月不会改变结肠细胞增殖的个人与结肠息肉或cancer.Implications的历史:β-胡萝卜素可能降低结肠癌发病率的机制似乎并不涉及或导致在正常结肠粘膜细胞增殖的变化,在个人与结肠息肉或癌症的历史研究。
Background: Epidemiologic studies have shown that consuming foods containing β-carotene is associated with a decreased incidence of colon cancer. The validity of this association has recently been questioned. It is not known if the rate of colonic cell proliferation differs among individuals with or without a history of colonic polyps or cancer and if proliferation changes in response to β-carotene.Purpose:This study was intended to (a) determine whether differences exist in colonic cell proliferation in individuals with and without prior colonic polyps or tumors, (b) demonstrate that β-carotene accumulates in colonic mu-cosa following dietary supplementation, and (c) determine whether mucosal P-carotene accumulation influences colonic cell proliferation.Methods:Subjects were enrolled in the phase I study from June 1991 until February 1994. The participants included 20 individuals (11 males and nine females, aged 62.3 ± 8.9 years [means ± SD]) with normal colons (as judged by recent colonoscopy), 40 (24 males and 16 females, aged 59.6 ± 10.1 years) with a history of colonic polyp(s), and 41 (30 males and 11 females, aged 67.2 ± 9.7 years) with prior colon cancer. The subjects in the last two groups consumed either 30 mg of β-carotene or placebo each morning for 3 months. This dose of β-carotene has no known toxic effects, but it can increase the serum level by approximately 10-fold. β-carotene concentration in serum and colonic tissue was quantitated by high-pressure liquid chromatography in samples collected before and after supplementation with β-carotene or placebo. Cellular proliferation was assessed on the basis of tissue ornithine decarboxylase activity, urinary polyamine excretion, and proliferating cell nuclear antigen expression. The differences in colonic cell proliferation parameters due to β-carotene supplementation, within and among different groups, were evaluated by the Wilcoxon matched-pairs signed ranked test and the Mann-Whitney test, respectively. All statistical tests were two-sided.Results:Colonic cell proliferation did not differ in samples obtained from individuals with and without prior colonic polyp(s) or cancer, β-carotene concentrations in serum and colonic tissue were significantly increased in groups receiving β-carotene (P<.001). However, cell proliferation did not differ, as judged by any of the three measures, among samples from all experimental groups collected before and after supplementation with β-carotene.Conclusions:Dietary supplementation with β-carotene for a period of 3 months does not alter colonic cell proliferation in individuals with a history of colonic polyps or cancer.Implications:The mechanism by which β-carotene might reduce colon cancer incidence does not appear to involve or result in a change in cell proliferation in the normal colonic mucosa as studied in individuals with a history of colonic polyps or cancer.