饵料维生素E含量对酸应激中华鳖幼鳖血清补体C3和C4的影响

为探讨维生素E(VE)对中华鳖(Pelodiscus sinensis)幼鳖血清补体C3和C4的影响及补体在酸应激下的变化,在6组(对照组,实验Ⅰ、Ⅱ、Ⅲ、Ⅳ和Ⅴ组)幼鳖的饵料中依次添加0、50、250、500、1000和5000mg／kg的VE,喂食4周,每组取半数幼鳖经酸应激处理24h。取幼鳖血清,用透射比浊法测定血清补体C3和C4的含量。经和未经酸应激的实验Ⅱ、Ⅲ和Ⅳ组幼鳖血清补体C3的含量均明显高于对照组,实验Ⅰ和Ⅱ组C4含量也明显高于对照组;经酸应激的幼鳖与未经酸应激的比较,对照组和实验Ⅰ组C3和C4的含量显著下降,其余4组没有变化。分析说明,VE在一定剂量范围内能促进血清补体C3和C4的合成,酸应激能导致其下降;而高剂量的VE对酸应激导致的不利影响有拮抗作用。     

维生素E对中华鳖幼鳖生长、肝脏维生素E以及血清皮质醇含量的影响

为探讨维生素E(VE)对中华鳖(Pelodiscus sinensis)幼鳖的生长、肝脏VE和血清皮质醇的影响，通过特定生长率、高压液相色谱法和放免法，我们测定了中华鳖幼鳖的生长、肝脏VE和血清皮质醇含量。发现VE添加量为1000和5000mg／kg的两组，能明显降低中华鳖幼鳖的生长。维生素E添加量为500、1000和5000mg／kg的三组，肝脏维生素E含量明显高于对照组，VE添加量在0—1000mg／kg的范围时，肝脏VE的含量随着饲料中VE含量的增加呈指数式增加，并且在VE添加量为5000kg／kg的一组基本达到饱和。维生素E添加量为0和50mg／kg的2组，其血清皮质醇的平均值明显高于维生素E添加量为250、500、1000和5000mg／kg的4组的平均值。上述结果表明：高剂量的VE降低了中华鳖幼鳖的生长和血清皮质醇的含量；在一定剂量范围内，肝脏VE随着饲料中VE含量的增加而升高。     

维生素C和E混合饲喂对中华鳖幼鳖抗酸应激能力的影响

来自甲鱼养殖场的60只中华鳖(Pelodiscus sinensis)幼鳖驯养3周后,实验设5组：对照组、处理Ⅰ、Ⅱ、Ⅲ和Ⅳ组。各组设2个平行,依次在饵料中混合添加维生素C(Vc)和E(VE)为0和0、250和50、2500和50、250和250、2500和250mg／kg,喂食4周后,每组取半数幼鳖经酸应激处理24h。取幼鳖血液,用镜检法测定血细胞的吞噬率,透射比浊法测定血清溶菌活力、杀菌活力以及补体C3和C4含量。①经酸应激与未经酸应激处理相比：对照组血细胞吞噬率显著降低,而处理Ⅰ-Ⅳ组无显著变化;对照组和处理Ⅰ组血清溶菌活力和补体C3含量显著下降,而处理Ⅱ-Ⅳ组无显著变化;血清杀菌活力均有显著下降(对照组、处理Ⅰ和Ⅲ组极显著,处理Ⅱ组和Ⅳ组显著);对照组、处理Ⅰ和Ⅲ组血清补体C4显著下降,而处理Ⅱ和Ⅴ组无显著变化。②经酸应激处理,血细胞吞噬率、血清溶菌活力、杀菌活力和补体C3含量,处理Ⅰ～Ⅳ组的均显著高于对照组,处理Ⅳ组显著高于其他4组;血清杀菌活力,处理Ⅱ组又高于处理Ⅰ和Ⅲ组;血清补体C4,对照组显著低于处理Ⅰ-Ⅳ组,而处理Ⅰ-Ⅳ组间无显著相异。Vc和VE混合饲喂对酸应激后中华鳖血细胞吞噬率、血清溶菌活力、杀菌活力和补体C3含量有显著协同促进作用,对血清补体C4的合成无协同作用。说明Vc和VE混合饲喂能显著增强中华鳖抗酸应激能力,缓解或部分缓解酸应激造成的不利影响。     

维生素C和E合用对中华鳖幼鳖非特异性免疫功能的影响

本研究旨在探讨维生素C和E合用对中华鳖幼鳖非特异性免疫功能的影响。实验设 5组 ,5组饵料中维生素C和E的添加量依次为 0和 0mg/kg(对照组 ) ;2 5 0和 5 0mg/kg(实验Ⅰ组 ) ;2 5 0 0和 2 5 0mg/kg(实验Ⅱ组 ) ;2 5 0和2 5 0mg/kg(实验Ⅲ组 ) ;2 5 0 0和 2 5 0mg/kg(实验Ⅳ组 )。喂食 4周 ,取其血液 ,测定中华鳖血细胞的吞噬率、血清溶菌活力、杀菌活力、补体C3和C4。结果表明 ,实验Ⅱ—Ⅳ组 ,血细胞吞噬率和血清杀菌活力明显高于对照组 ,实验Ⅳ组明显高于其他 4组 ,并且维生素C和E之间有明显的协同作用。血清溶菌活力和补体C3的含量 ,在实验Ⅰ—Ⅳ组明显高于对照组 ,实验Ⅳ组明显高于其他 4组。补体C4在实验Ⅰ—Ⅳ组明显高于对照组 ,但实验Ⅰ—Ⅳ组间没有明显差别 ,维生素C和E间也没有协同作用。     

维生素C和酸应激对中华鳖幼鳖血清补体C3和C4含量的影响

为研究维生素C对中华鳖(Pelodiscus sinensis)血清补体C3和C4的影响及其在酸应激条件下的变化,我们设置了6个实验组,饵料中维生素C的添加量依次为0、250、500、2500、5000和10000mg／kg,喂食4周后取其血清,用透射比浊法测定酸应激前后中华鳖血清补体C3和C4的含量。结果表明,维生素C添加量为250mg／kg时,血清补体C3的含量与对照组间没有明显不同;维生素C添加量为500、2500、5000和10000mg／kg的4组,血清补体C3的含量明显高于对照组和维生素C添加量为250mg／kg组;维生素C添加量为500mg／kg的一组,血清补体CA含量明显高于其它5组;维生素C添加量为250mg／kg组明显高于10000mg／kg组。酸应激后,补体C3的含量没有明显下降,将维生素C添加量为0、250和500mg／kg的三组并为一组处理,则应激后有明显下降。维生素C添加量为0、250和500mg／kg的3组,血清补体CA的含量在酸应激后明显下降,而维生素C添加量为2500、5000和10000mg／kg的3组,应激后血清补体C4没有明显变化。维生素C和酸应激对中华鳖血清补体C3和CA含量的影响没有交互作用。这说明,维生素C在一定剂量范围内,能提高中华鳖血清补体C3和CA的水平,酸应激能导致其含量降低,而高剂量的维生素C对其下降有颉颃作用[动物学报49(6)：769～774,2003]。     

维生素E对青鱼幼鱼生长、免疫及抗氨氮胁迫能力的影响

以初始体质量(7.270.40) g的青鱼为研究对象, 采用维生素E(VE)有效含量分别为14.36(对照组)、25.14、37.66、62.97、113.92和210.45 mg/kg 6种等氮等能的实验饲料, 饲养青鱼幼鱼8周后, 根据生长情况选取对照组、62.97和210.45 mg/kg VE组进行24h氨氮胁迫(20 mg/L), 研究VE对青鱼幼鱼生长、免疫及抗氨氮胁迫能力的影响。结果表明: 以特定生长率为指标, 折线模型分析表明青鱼有效维生素E需要量为45.00 mg/kg。肌肉、肝脏和血清VE含量与饲料中VE含量呈明显正相关, 当饲料VE含量超过113.92 mg/kg时, 肌肉和肝脏VE含量均达到饱和。VE对鳃丝Na+/K+-ATP酶活性(NKA)和血清皮质醇(COR)无显著影响, 但随着饲料VE含量的升高, 过氧化氢酶(CAT)和总超氧化物歧化酶活性(T-SOD)呈上升趋势, 丙二醛含量(MDA)呈下降趋势。氨氮胁迫对各处理组肌肉VE含量和血清CAT活性无影响, 但肝脏VE含量均显著降低(P0.05), 且62.97和210.4 5 mg/kg VE组血清VE水平有所升高。在胁迫后, 对照组血清T-SOD、鳃丝NKA活性显著降低, 皮质醇含量显著增加(P0.05)。与对照组相比, 62.97和210.45 mg/kg VE组T-SOD、NKA活性和皮质醇含量在胁迫前后无显著变化。各处理组MDA含量在胁迫后虽均显著升高, 但210.45 mg/kg VE组在胁迫后MDA含量仍显著低于对照组(P0.05)。以上结果说明, 青鱼幼鱼获得最大生长的有效维生素E需求量为45.00 mg/kg, 且较高VE能有效提高青鱼机体免疫力, 缓解氨氮胁迫对青鱼机体的负面影响。       

维生素E对TCDD染毒小鼠白细胞介素和T细胞亚群的影响

为研究维生素E(VE)对2,3,7,8四-氯代二苯并-对-二噁英(TCDD)染毒雄性小鼠白细胞介素(IL)和T细胞亚群的影响,我们设计了5个实验组,将40只小鼠随机分为5组,5组动物给予TCDD和维生素E的水平依次为:TCDD 0 ng/kg和VE0 mg/kg、TCDD 100 ng/kg和VE0 mg/kg、TCDD 100 ng/kg和VE20 mg/kg、TCDD 100ng/kg和VE100 mg/kg、TCDD 100 ng/kg和VE500 mg/kg。灌胃7周后取其血液和脾脏,用酶联免疫法测小鼠血清IL的水平,用流式细胞仪法测定脾脏T淋巴细胞亚群的变化。结果表明:TCDD染毒组小鼠血清IL-1α水平明显高于对照组;VE20 mg/kg和100 mg/kg的两组,其血清IL-1α水平均明显低于染毒组;而VE500 mg/kg组,其血清IL-1α水平与染毒组间差异没有统计学意义;TCDD染毒组小鼠血清IL-2水平明显低于对照组;VE100 mg/kg和500 mg/kg两组,其血清IL-2水平明显高于染毒组;TCDD染毒组CD4 T淋巴细胞百分比明显低于对照组;给予VE的三组,其脾CD4 T淋巴细胞百分比与TCDD染毒组相比有升高的趋势,但没有统计学意义;TCDD染毒组小鼠脾CD8 T淋巴细胞百分比明显高于对照组;VE为100 mg/kg组,其脾CD8 T淋巴细胞百分比明显低于染毒组和VE20 mg/kg两组;VE500 mg/kg组,其脾CD8 T淋巴细胞百分比明显低于染毒组。表明TCDD能导致机体白细胞介素分泌的紊乱以及脾脏T淋巴细胞亚群的变化,而适当剂量的VE对TCDD所致的毒性有拮抗作用。     

维生素C多聚磷酸酯对小鼠抗热应激能力的影响

为研究维生素C多聚磷酸酯对小鼠抗热应激能力的影响 ,将 4 8只 3～ 4周龄、体重为 16～ 2 9g的健康雄性小鼠随机分为 4组 (对照组、Ⅰ、Ⅱ和Ⅲ组 ) ,在其饵料中分别添加 0、 5 0 0、 2 5 0 0和 5 0 0 0mg/kg的35 %维生素C多聚磷酸酯。喂食 4周后 ,每组取一半小鼠处死取其肝脏 ,另一半置于 (35± 1)℃条件下 ,2 4h后作同样处理。用硫代巴比妥酸分光光度法测肝脏脂质过氧化物 (LPO)的含量 ,用亚硝酸盐形成法测超氧化物歧化酶 (SOD)的活性 ,用分光光度法测过氧化氢酶 (CAT)和谷胱甘肽过氧化物酶 (GSH Px)的活性。经热应激与未经热应激相比 ,LPO :对照组和Ⅰ组显著升高 ,而Ⅱ和Ⅲ组无显著差异。SOD和GSH Px :对照组显著下降 ,其他 3组无显著差异 ;其中SOD :Ⅱ和Ⅲ组显著高于对照组和Ⅰ组 ,GSH Px :Ⅲ组显著高于其他 3组。CAT :对照组和Ⅰ组显著降低 ,而Ⅱ和Ⅲ组无显著差异 ;Ⅱ和Ⅲ组显著高于对照组和Ⅰ组。表明热应激促进了小鼠肝脏LPO的产生 ,抑制了抗化物酶的活性 ;而维生素C多聚磷酸酯对热应激造成的不利影响有缓解作用。     

维生素E对黄鳝繁殖性能的影响

试验采用单因子梯度设计。在试验中,维生素E设6个梯度,分别为Ⅰ0mg／kg、Ⅱ50mg／kg、Ⅲ125mg／kg、Ⅳ200mg／kg、Ⅴ275mg／kg、Ⅵ350mg／kg,前后进行175d饲养试验,以雌鳝性腺系数、产卵力、孵化率以及各组织中SOD活性、MDA含量等指标作为判据,研究了VE对雌鳝繁殖性能的影响。结果表明,随饲料中VE含量的增加,Ⅰ、Ⅱ、Ⅲ、Ⅳ组雌鳝性腺系数、产卵力和孵化率显著提高(p0．05),Ⅴ、Ⅵ组则提高不显著(p0．05),卵中VE的含量反映了饲料中VE的含量。雌鳝卵巢中SOD活性,Ⅳ、Ⅴ和Ⅵ组比Ⅰ和Ⅲ组显著低(p0．05),相应地,MDA含量Ⅳ、Ⅴ和Ⅵ组显著低于Ⅰ、Ⅱ和Ⅲ组(p0．05)Ⅰ、Ⅱ和Ⅲ组雌鱔,虽然其卵巢中SOD活性较高,但因饲料中抗氧化性的VE缺乏或不足,引发卵子脂质过氧化,MDA含量显著升高(p0．05),导致卵质低下,从而影响了卵子孵化。综上所述,雌鳝饲料中添加维生素E,能有效地改善雌鳝的繁殖性能,其最适添加量为200mg／kg。       

外源维生素C及冬眠对中华鳖稚鳖生长、维生素C合成和肝脏维生素C含量的影响

本文研究了饲料中维生素C(Vc)对中华鳖稚鳖冬眠前后Vc合成能力及肝脏中Vc含量的影响。将体重为29.41g±5.44g的稚鳖180只,按其饲料中Vc含量(0、500、2500mgVc/kg饲料)分为Vc0、Vc500和Vc2500共3组,每组6个平行,每平行10只鳖。实验开始前称重得各组初始平均体重。25℃±1℃下用实验饲料饲喂4周后,缓慢降温至7℃,人工诱导其进入冬眠,此时为冬眠期开始,每组取6只鳖,称重后快速处死,取其肝脏和肾脏。其余鳖全部称重。冬眠8周末取样,处理同上。用高效液相色谱(HPLC)法测定肝脏Vc含量和肝脏、肾脏古洛糖酸内酯氧化酶(GLO)活力。结果发现中华鳖自身能够合成Vc,且合成部位在肾脏。饲喂4周不同Vc水平的饲料后,各组间特定生长率差异不显著。冬眠8周后,各组体重均有所降低,组间冬眠期间特定生长率无显著性差异。冬眠开始时,稚鳖肝脏Vc蓄积量有随外源Vc浓度升高而递增的趋势,但差异未达到显著性水平;经历冬眠后各组稚鳖肝脏Vc含量降低,Vc500组下降不显著,而Vc0与Vc2500组显著下降;肾脏GLO活力在不同Vc梯度组间及冬眠前后均无显著差异。以上结果表明:中华鳖冬眠过程中要消耗较多的肝脏Vc,外源Vc和冬眠对肾脏Vc合成能力影响不显著。     

The effect of maternal and cord-blood vitamin C, vitamin E and lipid peroxide levels on newborn birth weight

Background Newborn birth weight has been shown to significantly correlate with the blood levels of vitamin C. Objective This study was planned to answer the question of why vitamin C levels correlate with birth weight; does such correlation reflect a protective effect of vitamin C on fetal growth, by its antioxidant characteristics or does it correspond to the nutritional status of both the mother and the fetus. We examined the hypothesis that maternal blood levels of vitamin C, but not vitamin E influence newborn birth weight. We determined maternal and newborn blood levels of vitamin C, vitamin E, and lipid peroxides (an index of oxidative insult) and the birth weights of full-term newborns delivered at our hospital. Results Compared with maternal blood levels, newborns have higher levels of vitamin C and lipid peroxides, but lower levels of vitamin E. There was a significant correlation in levels between mothers and their newborns for blood levels of vitamin C (r = 0.82, P < 0.01) and vitamin E (r = 0.61, P < 0.02) but not for lipid peroxides (r = 0.001). This suggests that maternal vitamin C and vitamin E intake can influence fetal vitamin C and vitamin E levels. Linear regression analysis shows a significant positive relationship between newborn birth weight and maternal plasma vitamin C (r = 0.51, P < 0.02). Similarly, there was a modest but significant positive relationship between newborn birth weights and newborn vitamin C levels (r = 0.61, P < 0.05). However, there was no relationship between maternal or fetal vitamin E or lipid peroxides levels and the newborn birth weight. Conclusions This study with a small number of subjects suggests a significant association between newborn birth weight and maternal and newborn plasma vitamin C levels. Lack of relationship between birth weight and vitamin E and lipid peroxides suggest that antioxidant function of vitamin C does not appear to have a major role in the effect of vitamin C on birth weight.     

Kinetics of the reaction by which natural vitamin E is regenerated by vitamin C

The rate constant and activation energy of the regeneration reaction of natural vitamin E by vitamin C were determined with a double-mixing stopped-flow spectrophotometer. The formation of vitamin C radical was observed in the absorption spectrum. The kinetic effect of methyl substitution on the aromatic ring of vitamin E radical indicates that partial charge-transfer plays a role in the reaction. Since a substantial deuterium kinetic isotope effect was not found, the tunneling effect may not play an important role under the present experimental conditions.     

Influence of dietary vitamin E and C supplementation on vitamin E and C content and thiobarbituric acid reactive substances (TBARS) in different tissues of growing pigs

To investigate the influence and possible interactions of dietary vitamin E and C supplementation on vitamin content of both vitamins and oxidative stability of different pork tissues 40 Large White barrows from 25?kg to 106?kg were allocated to four different cereal based diets: Basal diet (B), dl-α-tocopherylacetate?+?200?mg/kg (E), crystalline ascorbic acid?+?300?mg/kg (C) or both vitamins (EC). At slaughtering samples of liver, spleen, heart, kidney, backfat outer layer, ham and M. longissimus dorsi were obtained. Growth performance of the pigs and carcass characteristics were not influenced by feeding treatments. Dietary vitamin E supplementation had a significant effect on the vitamin E and α-tocopherol concentration in all investigated tissues. Backfat outer layer, liver, spleen, kidney and heart had higher vitamin E concentrations than ham and M. longissimus dorsi. Dietary vitamin C supplementation tended towards enhanced vitamin E levels except for ham samples. Therefore, some synergistic actions without dietary vitamin E supplementation between the two vitamins could be shown. The vitamin C concentration and TBARS were increased or at least equal in all tissues due to vitamin C supplementation. Dietary α-tocopherol supplementation resulted in lower TBARS in backfat outer layer (malondialdehyde 0.35?mg/kg in B vs. 0.28?mg/kg in E), but increased in heart and ham. When both vitamins were supplemented (EC) TBARS were lower in M. longissimus dorsi and backfat outer layer, equal in heart and higher in liver and ham compared to a single vitamin C supplementation. Rancimat induction time of backfat outer layer was 0.3?h higher in C compared to B and 0.17?h higher in EC than in E. Correlations between levels of both vitamins were positive for kidney (r?=?0.169), M. longissimus dorsi (r?=?0.499) and ham (r?=?0.361) and negative for heart (r?=???0.350). In liver and spleen no interaction could be found. In backfat outer layer vitamin E was positively correlated with rancimat induction time (r?=?0.550) and negatively with TBARS (r?=???0.202), but provided no evidence that dietary vitamin E supply led to better oxidative stability.     

Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations

The exogenous antioxidants vitamin C (ascorbate) and vitamin E (α-tocopherol) often blunt favorable cell signaling responses to exercise, suggesting that redox signaling contributes to exercise adaptations. Current theories posit that this antioxidant paradigm interferes with redox signaling by attenuating exercise-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation. The well-documented in vitro antioxidant actions of ascorbate and α-tocopherol and characterization of the type and source of the ROS/RNS produced during exercise theoretically enable identification of redox-dependent mechanisms responsible for the blunting of favorable cell signaling responses to exercise. This review aimed to apply this reasoning to determine how the aforementioned antioxidants might attenuate exercise-induced ROS/RNS production. The principal outcomes of this analysis are (1) neither antioxidant is likely to attenuate nitric oxide signaling either directly (reaction with nitric oxide) or indirectly (reaction with derivatives, e.g., peroxynitrite); (2) neither antioxidant reacts appreciably with hydrogen peroxide, a key effector of redox signaling; (3) ascorbate but not α-tocopherol has the capacity to attenuate exercise-induced superoxide generation; and (4) alternate mechanisms, namely pro-oxidant side reactions and/or reduction of bioactive oxidized macromolecule adducts, are unlikely to interfere with exercise-induced redox signaling. Out of all the possibilities considered, ascorbate-mediated suppression of superoxide generation with attendant implications for hydrogen peroxide signaling is arguably the most cogent explanation for blunting of favorable cell signaling responses to exercise. However, this mechanism is dependent on ascorbate accumulating at sites rich in NADPH oxidases, principal contributors to contraction-mediated superoxide generation, and outcompeting nitric oxide and superoxide dismutase isoforms. The major conclusions of this review are: (1) direct evidence for interference of ascorbate and α-tocopherol with exercise-induced ROS/RNS production is lacking; (2) theoretical analysis reveals that both antioxidants are unlikely to have a major impact on exercise-induced redox signaling; and (3) it is worth considering alternate redox-independent mechanisms.     

Complexity of vitamin E metabolism

Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e., when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their sidechain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a supplement or nutrient. To evaluate individual vitamin E status, the analytical procedures used for detecting and quantifying vitamin E and its metabolites are crucial. The latest methods in analytics are presented.     

Physiological levels of tea catechins increase cellular lipid antioxidant activity of vitamin C and vitamin E in human intestinal caco-2 cells

Oxidative stress has been linked to the development of various chronic diseases. Vegetables and fruits, which contain polyphenols, were shown to have protective effects. (-)-Epigallocatechin-3-gallate (EGCG), a polyphenol abundant in tea, has been shown to have antioxidant activities in cell-free conditions and this study focused on the effect of cellular EGCG. Using an intestinal cell model to examine the oxidative stress induced by hydroxyl radicals, we report here that physiological concentrations (0.1-1 microM) of EGCG have dose- and incubation duration-dependent cell-associated lipid antioxidant activity (measuring malondialdehyde production). Vitamin E and vitamin C at 10-40 microM also showed cell-associated lipid antioxidant activities under shorter incubation durations. When EGCG was included in the incubation with vitamin E or C, more antioxidant activities were consistently observed than when vitamins were added alone. Catechin (widely present in fruits and vegetables) at 1 microM also significantly increased the antioxidant activity of vitamins E and C. Previous studies examining cell-associated activity of EGCG mainly focused on the 10-100 microM concentration range. Our results suggest that although the physiological level (0.1-1 microM) of dietary catechins is much lower than that of vitamins, they further contribute to the total antioxidant capacity even in the presence of vitamins.     

Membrane permeability changes with vitamin A/vitamin E mixed bilayers

Vitamin A (all trans-retinol) enhances the permeability of egg phosphatidylcholine liposomes to glucose, urea, and erythritol while vitamin E (α-tocopherol) decreases permeability to the same solutes. Egg phosphatidylcholine bilayers containing both vitamin A and vitamin E are shown to have an altered permeability more similar to that affected by vitamin E alone. The membrane stabilizing effect of vitamin E appears dominant over the membrane destabilizing effect of vitamin A.     

Photoprotective potential of lycopene, β-carotene, vitamin E, vitamin C and carnosic acid in UVA-irradiated human skin fibroblasts

The photoprotective potential of the dietary antioxidants vitamin C, vitamin E, lycopene, β-carotene, and the rosemary polyphenol, carnosic acid, was tested in human dermal fibroblasts exposed to ultraviolet-A (UVA) light. The carotenoids were prepared in special nanoparticle formulations together with vitamin C and/or vitamin E. Nanoparticle formulations, in contrast to dimethylsulphoxide, stablized lycopene in the cell culture medium and allowed efficient cellular uptake. The presence of vitamin E in the formulation further increased the stability and cellular uptake of lycopene. UVA irradiation of the human skin fibroblasts led to a 10–15-fold rise in metalloproteinase 1 (MMP-1) mRNA. This rise was suppressed in the presence of low μM concentrations of vitamin E, vitamin C, or carnosic acid but not with β-carotene or lycopene. Indeed, in the presence of 0.5–1.0 μM β-carotene or lycopene, the UVA-induced MMP-1 mRNA was further increased by 1.5–2-fold. This increase was totally suppressed when vitamin E was included in the nanoparticle formulation. Heme-oxygenase 1 (HO-1) mRNA expression was strongly induced by UVA irradiation but none of the antioxidants inhibited this effect at the concentrations used in this study. Indeed, β-carotene or lycopene (0.5–1.0 μM) led to a further 1.5-fold rise in the UVA-induced HO-1 mRNA levels. In conclusion, vitamin C, vitamin E, and carnosic acid showed photoprotective potential. Lycopene and β-carotene did not protect on their own but in the presence of vitamin E, their stability in culture was improved and the rise in MMP-1 mRNA expression was suppressed, suggesting a requirement for antioxidant protection of the carotenoids against formation of oxidative derivatives that can influence the cellular and molecular responses.     

Hematological and biochemical investigations on the effect of vitamin E and C on Oreochromis niloticus exposed to zinc oxide nanoparticles

This study was carried out to determine the LC₅₀ of zinc oxide nanoparticles (ZnONPs) on Oreochromis niloticus and to investigate the effect of vitamin E and C on hematological and biochemical alterations induced by two sublethal concentrations (1 and 2 mg/L) of ZnONPs. One hundred and eighty fish were used for studying the lethal concentrations of ZnONPs. For sublethal study two hundred and twenty-five males of O. niloticus were equally divided into five groups, control, the second and the third were treated with 1 and 2 mg/L ZnONPs respectively. The fourth and fifth were exposed to the same concentrations of ZnONPs plus vitamins E and C. The results revealed that the 96 h LC₅₀ of ZnONPs was 3.1 ± 0.4 mg/L. The sublethal study revealed the presence of normocytic normochromic anemia in groups (2, 3 and 5) along the experiment period. The 4th group showed normocytic normochromic anemia at the 7th day and microcytic hypochromic anemia at the 15th day. Leukocytosis, heterophilia, lymphopenia and monocytopenia were recorded at the 7th day in all treated groups compared with the normal control. At the 15th day heteropenia, lymphopenia and monocytopenia were reported in all treated groups. A significant increase in the serum levels of alkaline phosphatase, aminotransferases, urea, creatinine and erythrocytic nuclear and morphological abnormalities along the experimental periods in all treated groups compared with the normal control. Serum total protein and albumin levels were significantly decreased at the same period in the same groups. Addition of vitamin E and C to the diet (groups 4 and 5) significantly improved all measured parameters compared with groups (2 and 3) which treated with ZnONPs only.     

Effect of vitamin C and E supplementation in modulating the peripheral nerve conduction following cold exposure in humans

Exposure to an extremely cold environment without proper protection leading to hypothermia is an emergency, one of the several complications of which is impairment in nerve conduction. Our previous work in the rat model has shown the beneficial effect of vitamin C in modulating the effect of hypothermia on nerve conduction. The present study aimed to evaluate the effect of vitamins C and E, administered alone or in combination, in modulating the effect of mild hypothermia on human ulnar nerve conduction. The study was carried out on 26 volunteers divided into three groups: group I received vitamin C supplementation (2000 mg/day in a single dose and 1,000 mg/day for the next 6 days), group II received vitamins C and E in combination (1,000 mg and 800 mg respectively in a single dose and 500 mg and 400 mg respectively for the next 6 days) and group III received vitamin E (800 mg in a single dose and the same for the next 6 days). The recordings were carried out before and after single and weekly supplementation in each group. There was a fall in ulnar nerve conduction velocity with a reduction in the oral temperature of 2–2.5 °C. Vitamin C administered alone and in combination with vitamin E reduced the fall in ulnar nerve conduction velocity. Prior supplementation with vitamin C and E could help ameliorate the impairment in human ulnar nerve conduction due to hypothermia.