植物硒生理及与重金属交互的研究进展

硒是一种重要的微量元素,在低浓度时对生物有益,但高浓度时呈现与重金属类似的毒性。植物作为人体硒摄入的主要来源,其硒代谢对于植物硒积累乃至人体硒营养水平十分重要。研究植物硒吸收、代谢和积累机理能指导富硒粮食的生产,是解决人体硒摄入不足/超量问题的有效途径。本文在阐述土壤硒含量、形态、生物有效性及分布的基础上,综述了植物对硒的吸收、代谢机理的研究进展,并讨论了农业生物强化以及遗传育种生物强化等两种硒生物强化的实践方法,以及利用硒生物强化缓解重金属毒性减少积累;最后,提出了植物硒代谢及硒生物强化研究的前沿问题,以期为改善人体硒营养水平提高人体健康状况提供理论和实践依据。     

彩色小麦种质资源在生物强化和功能食品应用中的研究进展北大核心CSCD

因为人类膳食不平衡和微量营养缺乏导致的隐性饥饿已经受到国内外高度重视。利用生物育种技术培育富含各种微量营养的优良作物品种是生物强化和功能食品的主要发展方向。国内外大量研究表明,彩色小麦种质资源富含花青素、铁、锌、硒、维生素、叶酸等微量营养和蛋白质等,对抗炎、抗癌、糖尿病、心脑血管疾病、贫血病、生长发育不良等有一定的功效,将在保障粮食安全和人类健康中发挥重要作用。本研究首先介绍了隐性饥饿、生物强化、功能食品、功能农业和功能品种等方面的发展趋势,重点介绍了国内外彩色小麦种质资源功能营养成分及遗传育种方面的研究进展。建议广泛收集和创制彩色功能营养小麦新种质,挖掘优异营养基因资源,揭示彩色小麦花青素和微量营养(硒、锌、铬等微量元素,维生素,人体不能合成的8种氨基酸,叶酸等)以及品质(蛋白质含量和组分)性状的遗传耦合机理,以期为彩色小麦生物强化和主粮功能化提供理论依据和技术支撑。     

人体硒代谢与硒营养研究进展

硒是人体所必需的重要微量营养元素,综述了当前国内外人体硒代谢与硒营养的研究进展,包括硒源形式与吸收、人体的硒含量与分布、硒的代谢途径、硒的生物活化形式、硒与疾病、硒中毒和硒的安全摄入量。在此基础上,提出了针对我国硒资源分布、硒反应症分布和居民膳食结构硒摄入量的研究建议,为满足居民通过膳食和补充剂补硒预防和治疗疾病提供理论和实践指导。     

硒在植物保护与农产品质量安全中的应用进展

硒是人和动物所必需的微量元素,也是植物生长发育的有益元素。综述了硒在植物保护与农产品质量安全中的应用研究进展,包括硒在增强植物抗逆能力、延缓植物衰老、拮抗重金属毒性、降低农产品中硝酸盐累积量、缓解作物药害、减轻作物土壤连作障碍等方面的作用,并展望了硒在改善农产品营养品质和保障植物健康与农产品质量安全方面的应用前景和策略,以期为硒生物营养强化与植物保护及农产品质量安全关系的深入研究与实际应用提供参考。     

纳米硒的生物医学作用研究进展

硒是人体必需微量营养元素,在生命体中有延缓衰老、清除自由基、保护心血管、抗癌等诸多功效。但是,由于传统补硒剂的安全剂量和毒性剂量范围过于接近,导致硒在保健食品和医药品中的应用受到了限制。纳米硒是近些年来发展的一种新颖的硒形态,综述了纳米硒对生物体的毒性、生物医学作用(如抗氧化、抗癌、抗菌)、用作膳食营养补充剂的潜能等方面的研究进展,并对未来的研究进行了展望,以期为纳米硒的生物医学应用和保障人类的健康提供参考。     

作物铁生物强化

铁是植物必需的微量元素。缺铁不仅影响植物的生长,更影响作物的营养品质。铁营养摄入不足是导致人体缺铁性贫血的主要原因。在膳食结构中,以谷物为主食,特别是发展中国家的人群,缺铁性贫血更为严重。因此,以提高作物食用部分铁含量为目标的"铁生物强化"意义重大。首先,介绍了植物铁吸收、转运和储存的分子机制;其次,总结了提高作物铁含量和生物有效性的方法 ;最后,对未来作物铁生物强化的研究方向提出了展望。     

植物硒吸收转化机制及生理作用研究进展

硒是大多微生物、动物及人类的必要微量元素,但其在植物生长发育中的生理作用至今存在争议.较低浓度硒具有促进植物生长、提高植物耐受能力的功能,而大部分植物在高浓度下表现出中毒现象.随着人类对摄入硒及环境硒污染问题的认识加深,作物硒生物强化与硒污染植物修复问题引起重视,推动了对硒在植物中的吸收积累及代谢调控的研究.近年来对植物硒吸收及转化的研究表明,不同硒水平下植物对硒吸收积累及生理响应存在差异,土壤环境因素对植物硒吸收及转化具有重要影响,对高聚硒植物硒代谢研究逐渐揭示出硒在植物体内的转化过程和调控机理等.本文总结了目前硒生物强化与植物修复方面的研究进展,对环境中硒分布特点、植物硒吸收及其影响因素、植物体内硒转化及其过程调控关键酶,以及硒在植物中的生理作用等进行了综述,并对植物硒生理及分子机制未来研究方向进行展望.     

硒的生理功能、摄入现状与对策研究进展

硒是谷胱甘肽过氧化物酶、甲状腺素脱碘酶、硒蛋白K、硒蛋白W等多达25种硒蛋白的重要组分,与抗氧化、激素调节、矿质元素代谢等功能密切相关。综述了近10年来国内外对微量元素硒在人体中的生理功能、参考摄入量标准、硒摄入不足所导致的"硒隐性饥饿"问题的现状及其相应的对策等方面的研究进展,以期为硒的营养强化研究提供参考。     

叶酸在肠道疾病防治中的作用

叶酸是B族维生素之一,由蝶啶、对氨基苯甲酸和1个或多个谷氨酸结合而成,对人体正常生理活动和疾病防治特别是防治肠癌具有极其重要的意义。本文简要综述叶酸的吸收和代谢、叶酸对表观遗传的影响和叶酸在肠道疾病防治中的作用。     

硒生物营养强化小麦在发芽过程中的生理特征研究

选取硒生物营养强化种植获得的小麦品种扬麦16的低硒组A(硒含量5.245μg/g)、高硒组B(硒含量47.850μg/g)和非强化组CK(硒含量0.039μg/g)为研究对象,通过监测发芽过程中的发芽参数(芽长、根长、发芽率)、芽体的总硒和硒形态、酶[淀粉酶(AMS)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)]活力、总抗氧化能力(T-AOC)以及过氧化氢(H2O2)、丙二醛(MDA)含量的变化,探讨硒生物营养强化转化的内源硒对小麦发芽过程生理行为的影响。结果显示,内源硒对麦芽的根长、芽长没有明显影响,但适宜浓度的内源硒有助于提高小麦的发芽率。高硒小麦籽粒可以通过发芽过程将部分内源硒代蛋氨酸(Se Met)转化为硒代胱氨酸(Se Cys2)。内源硒有助于增强α-淀粉酶、抗氧化酶(GSH-Px和SOD)的活力,同时,可提高麦芽的总抗氧化能力(T-AOC)、降低麦芽体内H2O2和MDA的积累。     

Supra-physiological folic acid concentrations induce aberrant DNA methylation in normal human cells in vitro

The micronutrients folate and selenium may modulate DNA methylation patterns by affecting intracellular levels of the methyl donor S-adenosylmethionine (SAM) and/or the product of methylation reactions S-adenosylhomocysteine (SAH). WI-38 fibroblasts and FHC colon epithelial cells were cultured in the presence of two forms of folate or four forms of selenium at physiologically-relevant doses, and their effects on LINE-1 methylation, gene-specific CpG island (CGI) methylation and intracellular SAM:SAH were determined. At physiologically-relevant doses the forms of folate or selenium had no effect on LINE-1 or CGI methylation, nor on intracellular SAM:SAH. However the commercial cell culture media used for the selenium studies, containing supra-physiological concentrations of folic acid, induced LINE-1 hypomethylation, CGI hypermethylation and decreased intracellular SAM:SAH in both cell lines. We conclude that the exposure of normal human cells to supra-physiological folic acid concentrations present in commercial cell culture media perturbs the intracellular SAM:SAH ratio and induces aberrant DNA methylation.     

Experiments on the biological activities of various fractions of the folic acid antagonist "X-methyl" folic acid

A crude synthetic preparation called crude "X-methyl" folate has previously been shown to function as a folate antagonist for rats and chicks. This product has been shown to contain two folate antagonists: 9-methyl folate, present as 6% by weight of the product and which has low activity as a folate antagonist for Streptococcus faecalis, and pyrrofolic acid, a compound present in small amounts (0.04%), but having high anti-folate biological activity for S. faecalis. These experiments deal with the antifolate activity of these two fractions for the rat as measured by their effects on histidine oxidation. Rats were fed a purified diet based on 20% vitamin-free casein and containing 1.0% sulfasuxidine. When this diet was supplemented with a marginal amount of folic acid (0.3 mg per kg diet), the addition of 4 g of crude antagonist decreased histidine oxidation and decreased liver folate levels. The addition of 240 mg of pure 9-methyl folic acid (amount of 9-methyl folic acid in 4 g of crude) produced similar decreases in histidine oxidation and liver folate levels. A concentrate of pyrrofolic acid (equivalent to 4 g of crude) free of 9-methyl folic acid produced no decrease in histidine oxidation and minimal changes in liver folate. This indicates that the folate antagonist activity observed previously with animals is probably due to the 9-methyl folic acid component rather than to the pyrrofolic acid activity.     

Effect of high levels of dietary folic acid on folate metabolism in vitamin B12 deficiency

The effect of administering high levels of folic acid to vitamin B12-deficient animals was studied. In B12 deficiency histidine oxidation is decreased. This is the result of both decreased liver folate levels and increases in the proportion of methyltetrahydrofolates. The purpose of this study was to determine if the addition of very high levels of folic acid to B12-deficient diets could increase liver folates and thereby restore histidine oxidation. Rats were fed a soy protein B12-deficient diet containing 10% pectin which has been shown previously to accelerate B12 depletion. When this diet was supplemented with B12 and folic acid, histidine oxidation was 5.4% in 2 h and the livers contained 3.49 micrograms of folate/g. In the absence of B12, the histidine oxidation rate was 0.34% and the liver folate level was 1.33 micrograms/g. When 200 mg/kg of folic acid was added to the B12-deficient diet there was no increase in histidine oxidation (0.35%) but the liver folates were increased to 3.68 micrograms which is about the same as that with B12 supplementation. The percentage tetrahydrofolate of the total liver folates was the same with and without a high level of dietary folic acid. Thus there was an increase in the absolute level of tetrahydrofolate without any increase in folate function as measured by histidine oxidation. Red cell folate levels were the same with and without B12, which is in contrast to the markedly lower liver folate levels in B12 deficiency. These data suggest a difference between B12 regulation of folate metabolism in the liver and in the bone marrow.     

Formation of folates by microorganisms: towards the biotechnological production of this vitamin

Folates (vitamin B₉) are essential micronutrients which function as cofactors in one-carbon transfer reactions involved in the synthesis of nucleotides and amino acids. Folate deficiency is associated with important diseases such as cancer, anemia, cardiovascular diseases, or neural tube defects. Epidemiological data show that folate deficiency is still highly prevalent in many populations. Hence, food fortification with synthetic folic acid (i.e., folic acid supplementation) has become mandatory in many developed countries. However, folate biofortification of staple crops and dairy products as well as folate bioproduction using metabolically engineered microorganisms are promising alternatives to folic acid supplementation. Here, we review the current strategies aimed at overproducing folates in microorganisms, in view to implement an economic feasible process for the biotechnological production of the vitamin.

     

Effects of dietary folic acid level and symbiotic folate production on fitness and development in the fruit fly Drosophila melanogaster

Folic acid is a vitamin for probably all animals. When converted to folate forms, it is used in DNA synthesis and amino acid metabolism. Literature suggests insects must consume folates, folates do not affect others, is a toxin for some, and that a few insects synthesize it. It has been reported that Drosophila melanogaster does not consistently need dietary folate because it can synthesize it. This seems unlikely since animals generally lack this ability. More likely, folates thought to have been made by the fly came from microbial symbionts. We aimed to clarify how dietary folic acid affects fitness and development in fruit flies and whether flies may receive folates from microbial symbionts. We found larvae were more viable and developed faster with increasing dietary folic acid, with the surprising exception that larvae fed nearly-zero folic acid developed faster. Their body folate levels did not significantly differ from those that consumed up to 600 times more folic acid. However, these flies fed little folate only achieved normal body folate levels and development times when antibiotics were excluded from the diet. When flies consumed near-zero folates with antibiotics, their body folate levels decreased and development was prolonged. An assay for the endosymbiont Wolbachia in flies used to generate the experimental flies did not show presence of these bacteria. Our data suggest D. melanogaster can harbor unknown bacterial symbiont(s) that provide essential folates to their host when it is scarce in the diet, allowing the fruit fly to maintain growth and development.     

Evaluation of homocysteine,vitamin, and trace element levels in women with gallstones

ObjectiveIt was aimed to examine the changes in homocysteine, folic acid, and vitamin B12, which metabolize homocysteine from the body, and trace elements (zinc, copper, selenium, nickel) that affect the structure of tissues and epithelium in female patients with gallstone disease. Moreover, it was aimed to investigate the contribution of these selected parameters to the etiology of the disease and their usability in treatment according to the findings obtained.Materials and MethodsEighty patients, including 40 female patients (Group I) and 40 completely healthy female individuals (Group II) were included in this study. Serum homocysteine, vitamin B12, folate, zinc, copper, selenium, and nickel levels were evaluated. Electrochemiluminescence immunoassay was used in the analysis of vitamin B12, folic acid, and homocysteine levels, and the ICP-MS method was used in the analysis of trace element levels.ResultsHomocysteine levels in Group I were statistically significantly higher than in Group II. In terms of vitamin B12, zinc, and selenium, Group I levels were found to be statistically significantly lower than group II. There was no statistically significant difference between Group I levels and Group II in terms of copper, nickel, and folate.ConclusionIt was suggested that homocysteine, vitamin B12, zinc, and selenium levels should be determined in patients with gallstone disease and that vitamin B12, which is especially important in the excretion of homocysteine from the body, and zinc and selenium, which prevent the free radical formation and protect from its effects, should be added to the diets of these patients.     

Investigation of the effects of folate deficiency on embryonic development through the establishment of a folate deficient mouse model

BACKGROUND: Folic acid (FA) has been shown to reduce the incidence of neural tube, craniofacial, and cardiovascular defects and low birth weight. The mechanism(s) by which the vitamin is effective, however, has not been determined. Therefore, a folic acid deficient mouse model was developed. METHODS: To create a folic acid deficiency, ICR female mice were placed on a diet containing no FA and including 1% succinyl sulfathiazole (SS) for 4 weeks before mating. Control mice were fed diets with either: 1) FA and 1% SS [+SS only diet]; 2) FA [normal diet]; or 3) a breeding diet. Dams and fetuses were examined during various days of gestation. RESULTS: Blood analysis showed that by gestational day 18, plasma folate concentrations in the -FA+SS fed dams decreased to 1.13 ng/ml, a concentration approximately 3% of that in breeding diet fed dams (33.24 ng/ml) and 8% of that in +SS only/normal fed dams (13.59 ng/ml). RBC folate levels showed a similar decrease, whereas homocysteine concentrations increased. Reproductive outcome in the -FA+SS fed dams was poor with increased fetal deaths, decreased fetal weight, and delays in palate and heart development. CONCLUSIONS: Female mice fed a folic acid deficient diet and 1% succinyl sulfathiazole exhibited many of the characteristics common to human folic acid deficiency, including decreased plasma and RBC folate, increased plasma homocysteine, and poor reproductive outcomes. Thus, an excellent model has been created to investigate the mechanism(s) underlying the origin of birth defects related to folic acid deficiency.     

Folic acid supplementation inhibits NADPH oxidase-mediated superoxide anion production in the kidney

Hyperhomocysteinemia, a condition of elevated blood homocysteine (Hcy) levels, is a metabolic disease. It is a common clinical finding in patients with chronic kidney diseases and occurs almost uniformly in patients with end-stage renal disease. Hyperhomocysteinemia is also a risk factor for cardiovascular disease. Our recent studies indicate that hyperhomocysteinemia can lead to renal injury by inducing oxidative stress. Oxidative stress is one of the important mechanisms contributing to Hcy-induced tissue injury. Folic acid supplementation is regarded as a promising approach for prevention and treatment of cardiovascular disease associated with hyperhomocysteinemia due to its Hcy-lowering effect. However, its effect on the kidney is not clear. The aim of this study was to examine the effect of folic acid supplementation on Hcy-induced superoxide anion production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the kidney during hyperhomocysteinemia. Hyperhomocysteinemia was induced in male Sprague-Dawley rats fed a high-methionine diet for 12 wk with or without folic acid supplementation. A group of rats fed a regular diet was used as control. There was a significant increase in levels of superoxide anions and lipid peroxides in kidneys isolated from hyperhomocysteinemic rats. Activation of NADPH oxidase was responsible for hyperhomocysteinemia-induced oxidative stress in the kidney. Folic acid supplementation effectively antagonized hyperhomocysteinemia-induced oxidative stress via its Hcy-lowering and Hcy-independent effect. In vitro study also showed that 5-methyltetrahydrofolate, an active form of folate, effectively reduced Hcy-induced superoxide anion production via NADPH oxidase. Xanthine oxidase activity was increased and superoxide dismutase (SOD) activity was decreased in the kidney of hyperhomocysteinemic rats, which might also contribute to an elevation of superoxide anion level in the kidney. Folic acid supplementation attenuated xanthine oxidase activity and restored SOD activity in the kidney of hyperhomocysteinemic rats. These results suggest that folic acid supplementation may offer renal protective effect against oxidative stress.     

Folate biofortification in food plants

Folate deficiency is a global health problem affecting many people in the developing and developed world. Current interventions (industrial food fortification and supplementation by folic acid pills) are effective if they can be used but might not be possible in less developed countries. Recent advances demonstrate that folate biofortification of food crops is now a feasible complementary strategy to fight folate deficiency worldwide. The genes and enzymes of folate synthesis are sufficiently understood to enable metabolic engineering of the pathway, and results from pilot engineering studies in plants (and bacteria) are encouraging. Here, we review the current status of investigations in the field of folate enhancement on the eve of a new era in food fortification.