Institute of Inflammation and Repair, University of Manchester, Manchester, UK.
Am J Clin Nutr. 2013 Mar;97(3):646-52. doi: 10.3945/ajcn.112.049494. Epub 2013 Jan 30.
Skin cancer is a major public health concern, and the majority of cases are caused by solar ultraviolet radiation (UVR) exposure, which suppresses skin immunity. Omega-3 (n-3) PUFAs protect against photoimmunosuppression and skin cancer in mice, but the impact in humans is unknown.
We hypothesized that EPA-rich n-3 PUFA would abrogate photoimmunosuppression in humans. Therefore, a nutritional study was performed to assess the effect on UVR suppression of cutaneous cell-mediated immunity (CMI) reflected by nickel contact hypersensitivity (CHS).
In a double-blind, randomized controlled study, 79 volunteers (nickel-allergic women, 22-60 y old, with phototype I or II) took 5 g n-3 PUFA-containing lipid (70% EPA plus 10% DHA) or a control lipid daily for 3 mo. After supplementation, nickel was applied to 3 skin sites preexposed on 3 consecutive days to 1.9, 3.8, or 7.6 J/cm(2) of solar-simulated radiation (SSR) and to 3 unexposed control sites. Nickel CHS responses were quantified after 72 h and the percentage of immunosuppression by SSR was calculated. Erythrocyte [red blood cell (RBC)] EPA was measured by using gas chromatography.
SSR dose-related suppression of the nickel CHS response was observed in both groups. Photoimmunosuppression appeared less in the n-3 PUFA group than in the control group (not statistically significant [mean difference (95% CI): 6.9% (-2.1%, 15.9%)]). The difference was greatest at 3.8 J/cm(2) SSR [mean difference: 11% (95% CI: 0.5%, 21.4%)]. Postsupplementation RBC EPA was 4-fold higher in the n-3 PUFA group than in the control group (mean difference: 2.69% (95% CI: 2.23%, 3.14%), which confirmed the EPA bioavailability.
Oral n-3 PUFAs appear to abrogate photoimmunosuppression in human skin, providing additional support for their chemopreventive role; verification of study findings is required. This trial was registered at clinicaltrials.gov as NCT01032343.
皮肤癌是一个主要的公共卫生问题,大多数病例是由太阳紫外线(UVR)照射引起的,这种照射会抑制皮肤免疫。ω-3(n-3)多不饱和脂肪酸(PUFAs)可预防小鼠的光免疫抑制和皮肤癌,但在人类中的影响尚不清楚。
我们假设富含 EPA 的 n-3 PUFAs 会消除人类的光免疫抑制。因此,进行了一项营养研究,以评估通过镍接触超敏反应(CHS)反映的皮肤细胞介导免疫(CMI)对 UVR 抑制的影响。
在一项双盲、随机对照研究中,79 名志愿者(镍过敏女性,22-60 岁,皮肤类型 I 或 II)每天服用 5 克含 n-3 PUFAs 的脂质(70% EPA 加 10% DHA)或对照脂质,持续 3 个月。补充后,将镍应用于 3 个皮肤部位,这些部位在前 3 天连续暴露于 1.9、3.8 或 7.6 J/cm²的太阳模拟辐射(SSR)和 3 个未暴露的对照部位。在 72 小时后量化镍 CHS 反应,并计算 SSR 引起的免疫抑制百分比。通过气相色谱法测量红细胞[红细胞(RBC)]中的 EPA。
在两组中均观察到 SSR 剂量相关的镍 CHS 反应抑制。与对照组相比,n-3 PUFAs 组的光免疫抑制作用较小(无统计学意义[平均差异(95%置信区间):6.9%(-2.1%,15.9%)])。在 3.8 J/cm² SSR 时差异最大[平均差异:11%(95% CI:0.5%,21.4%)]。n-3 PUFAs 组补充后的 RBC EPA 比对照组高 4 倍(平均差异:2.69%(9 5%CI:2.23%,3.14%)),证实了 EPA 的生物利用度。
口服 n-3 PUFAs 似乎可消除人类皮肤的光免疫抑制,为其化学预防作用提供了额外支持;需要验证研究结果。该试验在 clinicaltrials.gov 上注册为 NCT01032343。