Effects of supplementation with vitamins A, C, and E, selenium, and zinc on immune function in a murine sensitization model

OBJECTIVE: We compared the effects of supplementing with vitamins A, C, and E, selenium, and zinc on a range of innate and specific T-helper 1 (Th1) and Th2-driven adaptive immune responses. METHODS: BALB/c mice were fed semi-purified AIN93 diets and randomly assigned to receive a diet supplemented with 120 mg/kg of vitamin A, 2500 mg/kg of vitamin C, 1000 mg/kg of vitamin E, 2 mg/kg of selenium, and 500 mg/kg of zinc (n = 15/group). After 4 wk of supplementation, mice were sensitized by topical application of di-nitro-chlorobenzene (DNCB); 2 wk later mice were challenged; and 5 d later they were killed to assess the effect on a range of innate responses (phagocytic activity, oxidative burst and tumor necrosis factor-alpha), adaptive Th1-driven responses (delayed-type hypersensitivity, DNCB-specific immunoglobulin [Ig] G2a and IgG2b, and interferon-gamma [IFN-gamma]), and adaptive Th2-driven responses (DNCB-specific IgE and IgG1 and interleukin-4 [IL-4]). RESULTS: Immune function was affected only in the vitamin A group. These mice gained less weight and were less capable of resolving the inflammatory response elicited during sensitization. The oxidative burst of blood cells was increased, but production of IFN-gamma and IL-4 and the ratio of IFN-gamma to IL-4 were markedly depressed. In concordance with the latter result, production of Th1-driven IgG2a antibodies was decreased, whereas Th2-driven isotypes were not affected (IgG1, IgE) and mucosal IgA was increased. CONCLUSIONS: These findings confirmed that supplementary amounts of vitamin A above dietary requirements enhance inflammatory responses accompanied by decreased Th1 and increased mucosal responses. However, supplementation of these sufficiently fed, non-stressed, young adult mice with vitamins C and E, selenium, or zinc had no effect on immune function. We speculate that using this model in aged, physiologically, or nutritionally stressed mice may provide outcomes more similar to those in sensitive human populations. If so, this would improve the usefulness of the model to assess, characterize, and rank effects of foods or nutrients on a range of immune functions, including Th1/Th2 polarization.     

硒维生素E和碘对营养性肥胖小鼠的影响

目的:探讨硒、维生素E和碘对营养性肥胖小鼠的影响。方法:先将小鼠随机分为普食对照组和营养性肥胖组,然后将营养性肥胖小鼠分为肥胖对照组、硒组、维生素E组、碘组、硒维生素E组和硒维生素E碘组,采用灌胃的方式给予硒、维生素E和碘,10周后检测体重、血糖、血清总胆固醇(TC)、血清甘油三酯(TG)、下丘脑瘦素、肝丙二醛(MDA)。结果:硒、维生素E和碘可减轻体重,降低血糖、TC、TG;下丘脑瘦素、肝MDA水平下降。结论:硒、维生素E、碘以及硒维生素E合用、硒维生素E碘合用均能降低肥胖小鼠体重、血糖、TC、TG,尤以硒维生素E碘合用效果为佳。     

维生素E、C和硒延缓衰老作用研究

<正> Harman的自由基学说认为,机体代谢过程中产生的自由基,通过损害机体细胞引起衰老。通常在正常生理状态下,机体内自由基的产生与清除处于动态平衡;自由基在不断产生的同时,又不断被清除自由基的酶系统(超氧化物歧化酶和谷胱甘肽过氧化物酶等)和非酶系统(维生素E、C和硒等)所清除。机体老化时,由于自由基清除能力降低而导致脂质过氧化物生成增强。自由基具有氧化膜脂质和损伤膜结构的作用。     

硒和维生素E对紫外线引起DNA损伤的保护作用

目的 研究硒和维生素E对由紫外线诱导的DNA损伤的保护作用。方法 体外培养人肺成纤维细胞。加硒和维生素E处理2h后，紫外线分别照射7，15，30min，然后用单细胞凝胶电泳技术检测细胞DNA的损伤情况。结果 经紫外线直接照射的细胞DNA损伤严重，而在照射过程中加入中浓度的硒或维生素E后细胞DNA损伤明显减轻。结论 紫外线照射细胞可使DNA受到损伤，硒和维生素E具有拮抗这种损伤的作用，可能与其抗氧化等功能有关。     

学龄儿童VA、VC、VE摄入水平对免疫功能影响

目的探讨膳食维生素A(VA)、维生素C(VC)、维生素E(VE)对儿童免疫功能的影响。方法选择河北省唐山市2所小学293名1~6年级学生进行一般情况、食物摄取频率和膳食调查,其中262名学生经家长知情同意后采静脉血测定免疫功能指标;营养计算器V1.6转换数据,SPSS 11.5统计软件进行分析。结果VA摄入水平为40%~20%推荐摄入量(RNI)时,CD4⁺、CD4⁺/CD8⁺、白介素-2(IL-2)、IgG及IgM分别为(27.83±12.38)%,1.23±0.12,(142.07±34.67)g/L,(10.49±0.47),(1.73±0.02)g/L,与参考值比较,差异均有统计学意义(P<0.01);VC摄入水平对CD3⁺、IgA及IgM有影响,当摄入水平分别低于100%和80%RNI时,CD3⁺、IgA低于参考值;低于60%RNI时,IgM高于参考值;当VE摄入水平低于120%、80%和80%适宜摄入量(AI)时,受其影响的CD4⁺、IL-2及IgG低于参考值。结论当VA摄入量≥120%RNI、VC摄入量≥120%RNI、VE摄入量≥160%AI时,对各免疫功能指标影响方能处于正常。     

维生素E和硒缺乏促进大鼠食管肿瘤发生及氧化应激机制的研究

目的探讨维生素E(VE)和硒(Se)营养缺乏对食管肿瘤发生的影响及其氧化应激机制。方法 110只雄性F344大鼠随机分为3组:VE/Se缺乏组,VE/Se正常组和溶剂对照组。VE/Se缺乏组和VE/Se正常组动物皮下注射N-甲基苄基亚硝胺(NMBzA)染毒,染毒剂量为0.35 mg/kg BW,每周3次,连续5周。溶剂对照组动物皮下注射等体积的20%二甲基亚砜(DMSO)。VE/Se缺乏组给予低VE/Se饲料(VE 46U/kg,Se 0.05mg/kg),VE/Se正常组、溶剂对照组给予正常饲料(VE 80U/kg,Se 0.15mg/kg)。在实验第25周解剖动物,进行食管肿瘤肉眼观察及病理检查。动物血浆VE水平采用高效液相色谱法检测,Se水平采用荧光法检测。食管组织中细胞增殖和DNA氧化损伤分别采用5-溴脱氧尿嘧啶(BrdU)和8羟基脱氧鸟苷(8-OH-dG)免疫组织化学法检测。动物血浆、食管及肝脏谷胱甘肽过氧化物酶(GPX)、谷胱甘肽转移酶(GST)活性采用试剂盒法检测。结果动物血浆VE和Se水平VE/Se缺乏组显著低于VE/Se正常组,VE/Se正常组略低于溶剂对照组。VE/Se缺乏组动物食管肉眼可见肿瘤发生率、平均肿瘤数量及病理损伤数量均显著高于VE/Se正常组(P<0.05);与VE/Se正常组相比,VE/Se缺乏组动物食管组织细胞增殖水平、8-OH-dG水平显著升高(P<0.05);动物血浆、食管及肝脏GPX和GST活性显著降低(P<0.05)。结论维生素E和硒缺乏能够加快细胞增殖,显著促进NMBzA诱发的大鼠食管肿瘤的发生,机体氧化应激、DNA氧化损伤在食管癌变过程中具有重要作用。     

Drink consumption in British preschool children: relation to vitamin C, iron and calcium intakes

Objective To examine the impact of soft drinks, fruit juices, milk and tea consumption on vitamin C, iron and calcium intakes in a large, representative sample of preschool children in the UK.
Design Secondary analysis of 4-day weighed dietary diaries.
Sample 1675 children aged 1.5–4.5 years living in the UK in 1992/993.
Results Fruit juice consumers, but not soft drink consumers, had higher vitamin C intakes and higher plasma ascorbate levels than nonconsumers ( P  < 0.001). However, overall intakes tended to exceed the RNI and 45% of children still had adequate intakes without the contribution of soft drinks and 56% without the contribution of fruit juice. Children who did not consume fruit juice or soft drinks were no more likely to have depleted levels of vitamin C than consumers. Tea drinkers had diets which were lower in iron and vitamin C than nonconsumers ( P  < 0.005). They had lower levels of haemoglobin ( P  < 0.05) but not ferritin. Children under 4 years old were less likely to meet the RNI for iron if they were tea drinkers ( P  < 0.005) but no more likely to be anaemic. Calcium intakes were significantly higher for whole milk consumers than for nonconsumers ( P  < 0.005) and 73% of overall calcium intake was predicted by quantity of all milks consumed. Whole milk consumers both under and over 4 years of age were significantly more likely to reach the RNI for calcium ( P  < 0.00005 and P  < 0.05).
Conclusions Preschool children's drinking has an impact on their intakes of vitamin C, iron and calcium. In particular, intakes of calcium are closely linked to the amount of milk consumed in this age group.     

Supplementation of vitamins C and E increases the vitamin E status but does not prevent the formation of oxysterols in the liver of guinea pigs fed an oxidised fat

Summary Background Dietary oxidised fats are a source of oxidative stress. They cause deleterious effects in animal organism by lowering the antioxidant status of tissues and enhancement of the formation of lipid oxidation products. The vitamins E and C might be useful to prevent the formation of oxidation products by dietary oxidised fats. Aim of the study The purpose of this study was to investigate whether or not supplementation of diets with vitamins E and C is able to prevent oxidative stress and the formation of lipid oxidation products caused by dietary oxidised fats. Among lipid oxidation products, oxysterols should be particularly considered because of their high pathophysiological effects. Methods Male guinea pigs were divided into five groups. Four groups were fed diets with an oxidised fat supplemented with 35 or 175 mg -tocopherol equivalents/kg and 300 or 1000 mg of vitamin C/kg for 29 days. One group, used as a control, was fed the same basal diet with fresh fat with 35 mg -tocopherol equivalents/kg and 300 mg of vitamin C/kg. Results The guinea pigs fed the oxidised fat diet with 35 mg -tocopherol equivalents/kg and 300 mg vitamin C/kg had significantly lower concentrations of tocopherols in various tissues, higher concentrations of various oxysterols and thiobarbituric acid-reactive substances in the liver, higher concentrations of glutathione in the liver and lower concentrations of glutathione in erythrocytes than the control animals fed the fresh fat. Increasing the dietary vitamin E concentration from 35 to 175 mg -tocopherol equivalents/kg and/or the dietary vitamin C concentration from 300 to 1000 mg/kg increased tissue tocopherol concentrations in guinea pigs fed the oxidised fat but did not influence concentrations of oxidation products in the liver and glutathione concentrations in liver and erythrocytes. Conclusion The results demonstrated that supplementation of vitamins E and C improves the vitamin E status but does not prevent the formation of lipid oxidation products in the liver of guinea pigs fed oxidised fats.     

膳食维生素B_6对硒的生物利用率影响的研究──Ⅲ．对成年大鼠组织中硒和谷胱甘肽过氧化物酶水平的影响

１２周龄雄性大鼠饲缺维生素Ｂ６（ＶＢ６）缺硒酪蛋白蔗糖基础膳食，３周后按体重把动物分成６组。分别喂饲三种膳食，即基础膳食、基础膳食中补充硒０．２５ｍｇ／ｋｇ的亚硒酸钠或ＤＬ－硒蛋氨酸，在此基础上每种膳食又分为补充（２．５μｇ／ｇ）或不补充盐酸吡哆醇两组。实验期为１４周。补Ｖ８６各组的红细胞和骨骼肌中硒水平和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均显著高于相应缺ＶＢ６各组，ＶＢ６对饲亚硒酸钠大鼠肝硒和ＧＳＨ－Ｐｘ水平没有影响；但当补充硒蛋氨酸时，与补ＶＢ６大鼠相比缺ＶＢ６大鼠的肝硒水平较高而ＧＳＨ－Ｐｘ活性则显著降低。这些研究结果进一步证明，ＶＢ６与血浆硒的转运和硒的利用有关，并且可能参与了硒蛋氨酸在肝脏中的代谢过程。     

Effect of vitamin E,selenium and age on lipid peroxidation events in rat cerebrum

The effect of 8 and 20 weeks of dietary vitamin E (200 IU/kg diet) and/or selenium (0.2 ppm) supplementation or deficiency on oxidative processes in cerebrum of 1 and 15 month old male F344 rats was examined. After 8 weeks of treatment a 32-fold difference in plasma and a 3-fold difference in cerebrum alpha-tocopherol (a-T) level was found between vitamin E supplemented and deficient young rats. These differences were 1.8- and 1.5-fold, respectively, in old rats and increased to 8- and 2-fold differences, respectively, after an additional 12 weeks of treatment. Selenium deficiency had a significant effect on plasma glutathione peroxidase activity and a slight sparing effect on plasma a-T content. Endogenous lipid peroxides (thiobarbituric acid reactants present without incubation) in cerebrum were not correlated with a-T concentration or age. However, incubation of cerebrum homogenates with or without the addition of 0.1 mM Fe²⁺, 0.25 mM ascorbic acid, or 100 mg % acetaldehyde revealed that dietary vitamin E has a major role and selenium has a minor role in the protection against ex-vivo and possibly in vivo lipid peroxidation in cerebrum.     

维生素C和维生素E对糖尿病大鼠非酶糖化和过氧化反应的影响

以链脲佐菌素腹腔注射ＳＤ大鼠建立糖尿病动物模型，在纯营养素饲料配方中补充维生素Ｃ和／或维生素Ｅ，喂饲周，观察单独或联合补充维生素Ｃ、维生素Ｅ对糖尿病非酶糖化及过氧化的干预作用。结果显示维生素Ｃ和Ｅ联合补充可显著减少糖尿病大鼠血红蛋白、低「密度脂蛋白及肾脏皮质的糖化终产物（ＡＧＥｓ）含量，同时显著降低脂质过氧化产物丙二醛（ＭＤＡ）水平，单独补充维生素Ｃ或维生素Ｅ能显著降低糖尿病鼠血清及肾脏ＭＤＡ含量     

儿童维生素A与铁营养状况的相关性研究

目的了解中国儿童维生素A(VA)的营养状况、VA缺乏率、VA边缘缺乏率,研究血浆VA与铁营养状况的相关性。方法由2002年“中国居民营养与健康状况调查”的大样本中随机抽取380名3~12岁儿童,检测血浆VA含量,同时测定血红蛋白(Hb)、总铁结合力(TIBC)、铁蛋白(SF)及转铁蛋白受体(sTfR)。了解儿童VA营养状况,计算VA缺乏率、VA边缘缺乏率,研究VA与铁营养状况评价指标的相关性。结果受试儿童VA平均含量为(1·03±0·24)μmol/L,其中8·4%儿童VA缺乏,44·7%儿童VA边缘缺乏。血浆VA与Hb呈正相关(r=0·16986,P<0·01),与sTfR呈负相关(r=-0·12863,P<0·05),与TIBC、SF不相关。结论铁缺乏伴随VA边缘缺乏在中国儿童中普遍存在,VA与铁营养状况存在相关性。     

住院治疗中新生儿维生素A、D、E水平单中心现况调查

目的 调查河南安阳地区住院治疗中新生儿维生素A、D、E水平及相关影响因素,为早期防治维生素A、D、E缺乏提供科学依据。方法 选取2017年5月-2019年2月在安阳市人民医院新生儿科住院治疗的329例新生儿为研究对象。采用高效液相色谱法和液相串联质谱法检测新生儿维生素A、D、E。结果 1)新生儿维生素A水平为(0.17±0.09) mg/L,维生素D水平为(14.21±12.05) ng/ml,维生素E水平为(6.50±3.80) mg/L。2) 足月儿与早产儿的维生素A水平,不同性别新生儿的维生素D水平,高危儿与非高危儿的维生素E水平差异均有统计学意义(P＜0.05)。不同体重组维生素A、D、E水平差异无统计学意义(P＞0.05)。3) 维生素A亚临床缺乏,维生素D及维生素E缺乏比例较高。4) 不同季节出生的新生儿维生素D水平差异有统计学意义(P＜0.05)。孕末期3个月补充维生素D剂量≥400 U/d与＜400 U/d的新生儿维生素D水平差异有统计学意义(P＜0.05)。结论 河南安阳地区住院治疗中新生儿大部分存在维生素A、D、E缺乏,是否足月、是否为高危儿可能分别与维生素A、E水平有关。不同性别、季节及孕末期补充维生素D的剂量与维生素D水平有关。     

硒和抗坏血酸对砷致大鼠细胞毒性拮抗作用

目的 观察不同浓度的亚砷酸钠(NaAsO2)对体外培养的大鼠淋巴活性氧群(ROS)和细胞内脂质过氧化物(LPO)含量的影响,并探讨亚硒酸钠(NaSeO3)和维生素C对砷毒性的拮抗作用.方法 体外分离大鼠外周血淋巴细胞后,施加处理因素,在37℃条件下恒温培养,用2'7'-二乙酰二氯荧光素(DCFH-DA)染色法检测细胞内的ROS水平,用硫代巴比妥酸荧光法测定细胞内LPO含量.结果 NaAsO2浓度>10μmol/L时,ROS和乙二醛(MDA)含量明显高于对照组;用抗氧化剂预处理使细胞内ROS和MDA含量减少.结论 亚砷酸钠可引起细胞内氧化应激,抗氧化物可一定程度拮抗砷的细胞毒性作用.     

维生素E、维生素C在肥胖儿童中抗氧化作用的临床研究

目的：探讨VitE与VitC在肥胖儿中的抗氧化作用。方法：检测62例肥胖儿童服用VitE和VitC前后血浆VitE、VitC、红细胞超氧化物歧化酶（SOD）活性及过氧化脂质（LPO）水平，与对照组进行比较。结果：在肥胖儿童组，除LPO值明显高于对照组外（P＜0．01），血浆VitE和VitC及红细胞SOD值均低于对照组（P＜0．05），服药后VitE和VitC血浆含量未发生明显变化（P＞0．05），而SOD值高于服药前，LPO降低（P＜0．05）。结论：肥胖儿童患者可能存在抗氧化机能降低现象。     

维生素A与维生素E增强叶酸防畸效果的研究

为观察维生素A与维生素E能否增强叶酸的防畸效果 ,采用环磷酰胺致大鼠胎鼠发育畸形作为动物模型 ,孕鼠在孕期分别补充叶酸和叶酸 +维生素A +维生素E ,观察其防畸效果。结果显示孕鼠不补充叶酸和维生素、单独补充叶酸和联合补充叶酸、维生素A和维生素E使胎鼠脑膨出率分别为 87 2 7%、42 0 3%和 30 0 8% (P <0 0 1)。联合补充组与单独补充叶酸组相比 ,脑膨出率降低更为明显 (P <0 0 5 ) ,上枕骨骨化程度明显提高 (P <0 0 1) ,胎鼠平均体重增加 (P <0 0 5 )。结果提示叶酸、维生素A、维生素E有明显促进胚胎发育及拮抗环磷酰胺的致畸作用 ,且叶酸与维生素A、维生素E联合应用的作用明显优于单独补充叶酸     

67例儿童血清维生素A、D、E水平研究

目的了解婴幼儿血清维生素A、D、E水平状况,为临床诊治工作提供参考。方法以2013年1-3月在首都儿科研究所附属儿童医院保健门诊67名要求健康体检儿童作为研究对象,采用高效液相色谱检测血清维生素A、25羟维生素D[25(OH)D]、维生素E水平,收集其基本情况、喂养方式、体格等方面信息。结果 67名儿童中,男40例,女27例。维生素A水平为(0.23±0.07)mg/L,缺乏率34.3%,不同月龄段血清水平差异有统计学意义(F=5.866,P=0.001),随月龄增加血清维生素A缺乏率逐渐减少,0~4个月组最低[(0.17±0.04)mg/L],缺乏率高达68.8%;不同喂养方式血清维生素A水平差异有统计学意义(F=2.838,P=0.045),纯母乳喂养组血清水平偏低[(0.18±0.03)mg/L],缺乏率为60.0%。血清25(OH)D水平为(102.26±90.54)nmol/L,缺乏率为13.3%;不同喂养方式水平差异有统计学意义(F=2.951,P=0.038),纯母乳喂养婴儿仍偏低[(96.93±20.42)nmol/L],缺乏率较高为33.3%。血清维生素E水平为(10.09±2.76)mg/L,不足率仅为13.4%,未发现缺乏儿童,维生素E营养状况良好。结论婴幼儿维生素A、D营养状况不容乐观,应针对高危人群及时施加干预以预防维生素缺乏症的发生。     

儿童反复呼吸道感染与血清维生素A、D、E水平的相关性研究

目的 探讨儿童反复呼吸道感染与患儿血清维生素A、D、E水平的相关性研究,为临床治疗提供科学依据。方法 选取2015年在长春市儿童医院参加儿童保健,近3个月反复呼吸道感染病史患儿66例为病例组;选取前来参加儿童保健的健康儿童66例为对照组。用高效液相色谱法检测维生素A、D、E的水平。结果 不同年龄组儿童患反复呼吸道感染疾病的差异有统计学意义(χ²=13.516,P=0.001),病例组儿童血清维生素A水平和缺乏率明显低于对照组(t=3.536,P=0.001;χ²=16.901,P=0.000),病例组儿童血清25(OH)D、维生素E水平和缺乏率与对照组比较差异无统计学意义(P>0.05)。结论 反复呼吸道感染可能与维生素A缺乏有关,建议加强营养教育和宣传,指导儿童家长进行科学喂养,定期监测维生素A、D、E水平并适量补充维生素。     

The Effect of Vitamin E and Vitamin C Supplementation on LDL Oxidizability and Neutrophil Respiratory Burst in Young Smokers

Objective: The purpose of this study was to determine the effect of vitamin E and/or vitamin C supplementation on low-density lipoprotein (LDL) oxidizability and neutrophil (PMN) superoxide anion production in young smokers.

Methods: Thirty smokers with a <5 pack-year history were randomly assigned to take placebo; vitamin C (1 g/day); vitamin E (400 IU/day); or both vitamins in a double-blind fashion. Subjects took the supplements for 8 weeks. At weeks 0 and 8, blood was collected for isolation of LDL and PMN, and for antioxidant vitamin analysis. LDL was oxidized with a copper (Cu) catalyst, and oxidation was measured by formation of conjugated dienes over a 5-hour time course. Lag times and maximum oxidation rates were calculated from the time course data. PMN superoxide anion release was assessed by respiratory burst after stimulation with phorbol ester and opsonized zymosan, and their ability to oxidize autologous LDL following treatment with the above stimuli was measured with the conjugated diene assay.

Results: Subjects who received vitamin E alone had a significant increase in the lag phase of Cu-catalyzed LDL oxidation (week 0, 118 ± 31 min vs. week 8, 193 ± 80 min, mean ± SD, p < 0.05), whereas the vitamin C and placebo groups had no changes in LDL oxidation kinetics. The group receiving both vitamins E and C had a significant reduction in oxidation rate (week 0, 7.4 ± 2.3 vs. week 8, 5.1 ± 2.1, p < 0.05). There were no significant changes for any group in PMN superoxide anion production or PMN LDL oxidation after stimulation with either phorbol ester or opsonized zymosan. Plasma and LDL vitamin E concentrations were significantly increased in both groups that received vitamin E. The subjects who received vitamin C alone had no significant change in plasma vitamin C concentrations; however, when data were pooled from both groups who received vitamin C, the increases were significant.

Conclusion: Vitamin E supplementation of young smokers was effective in reducing Cu-catalyzed LDL oxidizability; however, vitamin E and/or C supplementation showed few significant effects on the more physiologically relevant PMN function. This casts doubt on the ability of antioxidant supplementation to reduce oxidative stress in smokers in vivo. Therefore, smoking cessation remains the only means by which young smokers can prevent premature coronary heart disease.