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膳食β-胡萝卜素与紫外线诱导的免疫抑制

Dietary beta-carotene and ultraviolet-induced immunosuppression.

作者信息

Noonan F P, Webber L J, De Fabo E C, Hoffman H A, Bendich A, Mathews-Roth M

机构信息

Department of Dermatology, George Washington University Medical Centre, Washington, DC 20037, USA.

出版信息

Clin Exp Immunol. 1996 Jan;103(1):54-60. doi: 10.1046/j.1365-2249.1996.905595.x.

DOI:10.1046/j.1365-2249.1996.905595.x
PMID:8565287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2200329/
Abstract

Ultraviolet (UV)-induced immunosuppression is a critical step in UV carcinogenesis, permitting tumour outgrowth. We investigated the effect of dietary beta-carotene on UV suppression of contact hypersensitivity (CHS) to trinitrochlorobenzene (TNCB) in BALB/c mice. Mice were fed for 10-16 weeks chow alone or supplemented with 1% beta-carotene or placebo as beadlets. Serum beta-carotene was detectable by high performance liquid chromatography (HPLC) analysis only in beta-carotene-fed mice (2.06 +/- 0.15 micrograms/ml). Serum retinol was 0.22-0.27 micrograms/ml in all three groups. Mice (n = 41/dietary group) were irradiated with 0, 4.5, 9 or 18 kJ/m2 of UVB and the CHS response was measured. Decreased CHS responses were observed in all UV-irradiated groups compared with unirradiated controls. UV dose-responses for suppression of CHS derived by first-order regression analyses of plots of percentage suppression of CHS as a function of log10UV dose showed significant slopes (P < 0.02) for all three dietary groups and similar residual variances between groups, P > 0.05. The UV dose for 50% suppression of CHS was 6.3 kJ/m2 for control, 6.4 kJ/m2 for placebo, and 5.5 kJ/m2 for beta-carotene-fed mice. No significant differences in slopes or elevations between UV dose-responses were observed, P > 0.05. Skin levels of the initiator of UV-induced immunosuppression, cis urocanic acid, were determined by HPLC in mice given 0 or 9 kJ/m2 of UV (n = 28/dietary group). No significant differences were observed between dietary groups (range 35.2-41.1 ng/mg skin, P > 0.15) We conclude feeding beta-carotene to BALB/c mice does not alter susceptibility to UV immune suppression, in contrast to human studies.

摘要

紫外线(UV)诱导的免疫抑制是UV致癌过程中的关键步骤,它使得肿瘤得以生长。我们研究了膳食β-胡萝卜素对BALB/c小鼠紫外线抑制三硝基氯苯(TNCB)接触性超敏反应(CHS)的影响。小鼠单独喂食普通饲料10 - 16周,或补充1%的β-胡萝卜素或作为小丸剂的安慰剂。仅在喂食β-胡萝卜素的小鼠中通过高效液相色谱(HPLC)分析可检测到血清β-胡萝卜素(2.06±0.15微克/毫升)。三组小鼠的血清视黄醇均为0.22 - 0.27微克/毫升。给小鼠(每组n = 41)照射0、4.5、9或18千焦/平方米的UVB,并测量CHS反应。与未照射的对照组相比,所有UV照射组的CHS反应均降低。通过对CHS抑制百分比作为log10UV剂量函数的图进行一阶回归分析得出的CHS抑制的UV剂量反应,在所有三个膳食组中均显示出显著斜率(P < 0.02),且组间残差方差相似,P > 0.05。CHS抑制50%时的UV剂量,对照组为6.3千焦/平方米,安慰剂组为6.4千焦/平方米,β-胡萝卜素喂养组为5.5千焦/平方米。在UV剂量反应之间未观察到斜率或截距的显著差异,P > 0.05。通过HPLC测定给予0或9千焦/平方米UV的小鼠(每组n = 28)皮肤中UV诱导免疫抑制的起始物顺式尿刊酸的水平。膳食组之间未观察到显著差异(范围为35.2 - 41.1纳克/毫克皮肤,P > 0.15)。我们得出结论,与人体研究相反,给BALB/c小鼠喂食β-胡萝卜素不会改变其对紫外线免疫抑制的易感性。

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