Dietary phytate,zinc and hidden zinc deficiency

Epidemiological data suggest at least one in five humans are at risk of zinc deficiency. This is in large part because the phytate in cereals and legumes has not been removed during food preparation. Phytate, a potent indigestible ligand for zinc prevents it's absorption. Without knowledge of the frequency of consumption of foods rich in phytate, and foods rich in bioavailable zinc, the recognition of zinc deficiency early in the illness may be difficult. Plasma zinc is insensitive to early zinc deficiency. Serum ferritin concentration ≤ 20 μg/L is a potential indirect biomarker. Early effects of zinc deficiency are chemical, functional and may be “hidden”. The clinical problem is illustrated by 2 studies that involved US Mexican-American children, and US premenopausal women. The children were consuming home diets that included traditional foods high in phytate. The premenopausal women were not eating red meat on a regular basis, and their consumption of phytate was mainly from bran breakfast cereals. In both studies the presence of zinc deficiency was proven by functional responses to controlled zinc treatment. In the children lean-mass, reasoning, and immunity were significantly affected. In the women memory, reasoning, and eye-hand coordination were significantly affected. A screening self-administered food frequency questionnaire for office might help caregiver's identify patients at risk of zinc deficiency.     

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Zinc (Zn) requirements are increased during lactation. Increased demand is partially met through increased Zn absorption from the diet. It is estimated that 60–80% of women of reproductive age are at risk for Zn deficiency due to low intake of bioavailable Zn and increased demands during pregnancy and lactation. How Zn is redistributed within the body to meet the demands of lactation, and how Zn deficiency affects this process, is not understood. Female C57bl/6J mice were fed a control (ZA; 30 mg Zn/kg) or a marginally Zn deficient (ZD; 15 mg Zn/kg) diet for 30 days prior to mating through mid-lactation and compared with nulliparous mice fed the same diets. While stomach and plasma Zn concentration increased during lactation in mice fed ZA, mice fed ZD had lower stomach Zn concentration and abrogated plasma Zn levels during lactation. Additionally, femur Zn decreased during lactation in mice fed ZA, while mice fed ZD did not experience this decrease. Furthermore, red blood cell, pancreas, muscle and mammary gland Zn concentration increased, and liver and adrenal gland Zn decreased during lactation, independent of diet, while kidney Zn concentration increased only in mice fed ZD. Finally, maternal Zn deficiency significantly increased the liver Zn concentration in offspring but decreased weight gain and survival. This study provides novel insight into how Zn is redistributed to meet the increased metabolic demands of lactation and how marginal Zn deficiency interferes with these homeostatic adjustments.     

Soil-sodicity-induced zinc deficiency in maize

Summary Maize (Zea mays L. cv. Ganga-2) plants were grown in pot culture on a loamy alluvial soil of Lucknow district (India) alkalinized to graded levels of ESP (Exchangeable Sodium Percentage) ranging from 15.5 to 55.3. Before sowing maize seeds the soil was fertilised with NPK, Fe, Mn and Cu. At and above ESP 34 Zn-deficiency symptoms first appeared at 30 days. The symptoms gradually became pronounced with increase in age and at 60 days they were found even at ESP 15.5. The severity of symptoms was related to increase in sodicity. Alkalinization of soils depressed available soil Zn and tissue Zn and increased tissue ratios of Na/Zn and P/Zn. It also decreased the total plant content of Zn, Fe, Mn, Cu and even Na. Increase in soil sodicity increased both tissue concentration and total content of P in plants upto ESP 34 beyond which it decreased it. Among different extractants, 0.1N HCl, DTPA pH 7.3 and EDTA-(NH₄)₂ CO₃ pH 8.6, for measuring available soil Zn the latter showed best correlations with soil ESP (−), tissue P (−), P/Zn ratio (−), dry matter yield (+) and tissue Zn (+). Tissue Zn was related to yield (+), tissue Na (−) and soil ESP (−). Mild, moderate, severe and very severe Zn deficiency in maize was induced by soil ESP levels, 18, 25, 33 and 45, respectively.     

Light-mediated release of phytosiderophores in wheat and barley under iron or zinc deficiency

The effect of varied light intensity (50 – 600 mol m-2 s-1) on the rate of phytosiderophore release was studied under zinc (Zn) deficiency using a bread (Triticum aestivum L. cv. Aroona) and a durum wheat cultivar (Triticum durum Desf. cv. Durati) differing in zinc (Zn) efficiency and under iron (Fe) deficiency using a barley cultivar (Hordeum vulgare L. Europe). Plants were grown under controlled environmental conditions in nutrient solution for 15 days (wheat plants) or 11 days (barley plants). Phytosiderophore release was determined by measuring capacity of root exudates to mobilize copper (Cu) from a Cu-loaded resin.With increasing light intensity visual Zn deficiency symptoms such as whitish-brown lesions on leaf blade developed rapidly and severely in wheat, particularly in the durum cultivar Durati. In wheat plants supplied well with Zn, increases in light intensity from 100 to 600 mol m-2 s-1 did not clearly affect the rate of phytosiderophore release. However, under Zn deficiency increases in light intensity markedly enhanced release of phytosiderophores in Zn-deficient Aroona, but not in Zn-inefficient Durati. When Fe-deficient barley cultivar Europe was grown first at 220 mol m-2 s-1 and then exposed to 600 mol m-2 s-1 for 24 and 48 h, the rate of release of phytosiderophores was enhanced about 4-fold and 7-fold, respectively. Transfer of Fe-deficient plants from 600 to 50 mol m-2 s-1 for 48 h reduced the rate of release of phytosiderophores by a factor of 7. The effect of light on phytosiderophore release was similar regardless of whether the rate of phytosiderophore release was expressed per plant or per unit dry weight of roots.The results demonstrate a particular role of light intensity in phytosiderophore release from roots under both Zn and Fe deficiency. It is suggested that in the studies concerning the role of phytosiderophore release in expression of Zn or Fe efficiency among and within cereals, a special attention should be given to the light conditions.     

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

INTRODUCTIONZinc is essential for normal brain development,evidenced by the fact that zinc deficiency in lactating mothers is characterized by a high incidence ofneuroanatomical maiformatinns and functional abnormalities in suckling offspring[1-3]. By colltrast,relatively little is known about the relationship be{tween maternal zinc nutrition and fetal brain development[2, 4, 5]. Dvergsten et al[6-81 investigated theeffects of maternal zinc deficiency on postnatal development of the rat ce…     

Non-destructive measurement of wheat roots in large undisturbed and repacked clay soil cores

Summary Non-destructive observations of root growth and distribution can be obtained from counting root intercepts with observation tubers inserted in the root zone. This paper describes the technique of inserting clear acrylic tubes horizontally into large undisturbed and repacked soil cores. Counts of roots intersecting scribed lines on the sides of the tubes were made with a fibrescope. Comparison was made between observation root tubes of different diameter (25 and 38.5 mm).The r² values for the relationships between root intercept counts and destructively determined values of root length density (RLD) ranged from 0.78 to 0.96. The larger diameter tubes had higher r² values. Theoretical calibration of the technique does not appear to be possible since analysis indicated that fewer roots intersected the scribed lines on the observation tube than would have been expected from a non-disturbed, randomly distributed root system. It is not known if this discrepancy is due to non-randomness or to an artifact associated with the insertion of the observation tube. Roots were not more prolific at the edge of the soil cores. Comparison of values of root length per unit soil surface area, rates of downward root growth and water uptake rates were within the ranges previously reported for wheat roots of field crops grown on clay soils. Observed root growth and distribution was found to be sensitive to four soil and water treatments imposed. It is concluded that the technique will allow quantitative analysis of root growth and distribution in undisturbed soil cores.     

Effects of maternal marginal zinc deficiency on myelin protein profiles in the suckling rat and infant rhesus monkey

In the current study, the effects of marginal Zn deficiency on myelin protein profiles in neonatal rats and rhesus monkeys were investigated. Following mating, rats were fed a Zn-adequate diet,ad libitum (50 μg Zn/g; 50 Zn AL), or a marginal Zn diet (10 μg Zn/g) from day 0 (10 Zn d0) or day 14 (10 Zn d14) of gestation to day 20 postnatal. An additional group of dams was restricted-fed the control diet to the food intake of the 10 Zn d0 group (50 Zn RF). Day 20 pup plasma and liver Zn concentrations in the 10 Zn groups were lower than in the 50 Zn groups. In a parallel experiment, rhesus monkeys were fed a Zn-adequatead libitum diet (100 μg Zn/g) or a marginal Zn diet (4 μg Zn/g diet; MZD) throughout gestation and lactation. Day 30 monkey infant plasma and liver Zn levels were similar in the MZD and control groups. Rat brain and monkey brain cortex weights were similar among the dietary groups. The amount of myelin recovered (mg protein/g brain) from day 20 rat pups from the 10 Zn groups was lower than that recovered from the 50 Zn rat pups. Myelin recovery from the MZD and control monkey infants was similar. When myelin protein profiles were characterized, it was found that the percentages of high-molecular-weight (HMW) proteins and Wolfgram protein were higher, whereas the percentages of small and large basic proteins were lower in myelin from the 10 Zn d0 and 50 Zn RF pups compared to the distribution in the 50 Zn AL rat pups. Results for the 10 Zn d0 and 10 Zn d14 pups were similar for all of the parameters studied. The percentage of HMW proteins was higher and that of basic protein lower in myelin from MZD monkey infants compared to the percentage of these proteins in myelin from controls. Although the interpretation of the rat data is complicated because of the anorexia associated with the Zn deficiency, the observed changes in monkey myelin protein profiles provide strong evidence that maternal Zn deficiency affects myelination in the offspring.     

Daily zinc supplementation effect on zinc deficiency in rats during prolonged restriction of motor activity

The objective of this investigation was to evaluate the effect of 47 mg zinc supplementation on deficiency of zinc in rats during 98 d of restriction of motor activity (hypokinesia), which appeared by higher plasma zinc concentration. One Hundred 13-week-old Sprague-Dawley male rats weighing 360–390 g were used to perform the studies: They were equally divided into four groups: 1. Unsupplemented control animals (UCA); 2. Unsupplemented hypokinetic animals (UHA); 3. Supplemented control animals (SCA); and 4. Supplemented hypokinetic animals (SHA). For the simulation of the effect of hypokinesia (HK), the UHA and SHA were kept in small individual cages made of wood, which restricted their movements in all directions without hindering food and water intake. The SCA and SHA received daily with their food an additional amount of zinc. Before and during the experimental period of 98 d, plasma, urinary and fecal zinc, balance of zinc, food intake, and body weight were determined at different intervals. In the SHA and UHA, the concentration of zinc in plasma, and the elimination of zinc in urine and feces increased significantly when compared with the SCA and UCA, whereas the balance of zinc was negative. The body weight and food intake decreased significantly in the SHA and UHA when compared with the SCA and UCA. The increased plasma concentration of zinc in both the SHA and UHA groups was in contrast to the observed hypozincnemia during prolonged immobilization as during prolonged hospitalization. This reaction suggests that there may be some other mechanisms that are affecting the process of control and regulation of zinc metabolism during prolonged HK. It was concluded that exposure to prolonged restriction of motor activity of rats induces significant increases in plasma concentration, fecal and urinary elimination of zinc in the presence of negative zinc balance and regardless the daily intake of large amounts of zinc with their food, leading to zinc deficiency.     

Aorta protein networks in marginal and acute zinc deficiency

Human zinc deficiency is a global problem and may influence the development of cardiovascular disease. Our objective was to determine Zn deficiency affected pathways and protein interactions in rat aorta and their likely influence on stress-induced atherogenesis. In two separate studies, rats were given diets acutely (<1 mg Zn/kg) or marginally (6 mg Zn/kg) deficient in Zn. Both studies included Zn adequate controls (35 mg Zn/kg) and the acute deficiency study included a pair-fed group. After 6 wk, proteins from thoracic aorta were separated by 2-DE. Proteins affected by zinc deficiency were identified by principal component analysis. Multiple correlations of identified proteins indicated protein networks of related function. Proteins clusters decreased in zinc deficiency were related to fatty acid and carbohydrate metabolism. Structurally related proteins, including zyxin and over nine transgelin 1 proteins, were either increased or decreased by acute and marginal deficiencies. PKC alpha was significantly decreased in Zn deficiency suggesting that Zn may regulate the phosphorylation of target proteins. Zn deficiency-related changes in structural, carbohydrate and fatty acid-related proteins may be disadvantageous for maintaining vascular health and are consistent with a protective role for zinc in the development of atherosclerosis.     

缺磷胁迫下的小麦根系形态特征研究

研究了缺磷条件下不同基因型小麦（Triticum aestivum L.)苗期根系形态学适应特征,以明确环境因子对根系不同组分（根轴和侧根）生长发育调控作用的强度和根系形态与磷营养效率关系。在缺P环境中,小麦根轴数量和侧根长度明显减小,同化物向根部的分配比例增加,根轴长度、侧根数量和根系长度等均有显著提高。供试基因型小麦的根轴数量及其长度的差异在每个供磷水平及不同供磷水平之间均呈显著,说明这两种性状的差异是由基因型和环境因素共同决定的;而侧根特征的差异只在不同供磷水平间显著,表明侧根性状主要受环境因素的控制。对6种基因型小麦的研究表明,根轴数量、根轴长度、根生长角度和根系长度根角之间存在着显著的基因型差异。相关分析表明,小麦的相对产量与缺磷条件下的小麦苗期根系形态指标的交互作用之间具有显著的线性关系。这种关系说明根系形态性状可作为早期有效地筛选磷高效小麦品种的指标。     

Effects of zinc deficiency and supplementation on plasma leptin levels in rats

The effects of zinc deficiency and supplementation on plasma leptin levels were studied in Sprague-Dawley rats. After 6 wk on a zinc-deficient diet containing 0.65 ppm Zn/g, the mean body weight was significantly lower than that of normal or zinc-supplemented rats, which showed no difference among them. The plasma leptin and zinc levels were lowest in zinc-deficient animals and highest in those that received a normal diet and daily intraperitioneal injections of 3 mg Zn/kg. These results indicate that zinc deficiency leads to a significant inhibition in plasma leptin levels, whereas zinc supplementation significantly increases plasma leptin.     

P、Zn在小麦细胞内的积累、分布及交互作用的研究

报道了小麦无性系细胞在含有3个P水平(0.5、1.5、3.5mmol·L^-1)和2个Zn水平(0、60μmol·L^-1)的M.S培养液中,细胞对P、Zn的积累、分布特性及交互作用的研究.P和Zn在细胞内的积累分别随外施P、Zn浓 度的提高而提高.与缺Zn比较,加Zn处理能抑制培养7d细胞中P的含量.营养液中0.5～1.5mmol·L^-1 P能促进细胞的含Zn量,但高P处理即抑制细胞的含Zn量.小麦细胞壁固定了细胞83.9%～88.3%的P,而外施P浓度越高,则细胞壁中P分配的比例越大.在供Zn条件下,细胞壁截留了细胞中一半以上的Zn(52.0～60.5%).小麦液泡中P和Zn的含量较少,分别为2.2%～3.8%和10.6%～30%.     

Increase in hippocampal cell death after treatment with kainate in zinc deficiency

Susceptibility to kainate-induced seizures is enhanced by zinc deficiency. To evaluate kainate-induced excitotoxicity in zinc deficiency, the relationship between kainate-induced seizures and hippocampal cell death was examined in control and zinc-deficient mice. Mice were fed a control and zinc-deficient diet for 4 weeks, and then intraperitoneally injected with 12 mg/kg kainate every 60 min three times. The rate of dead mice to the total mice was higher in zinc-deficient group than in control group 3 days after the last injection of kainate. In the survivals, which exhibited tonic convulsions in both control and zinc-deficient groups, kainate-induced hippocampal cell death was also analyzed by cresyl violet staining. Neuronal loss was more observed in the CA1, CA2 and CA3 pyramidal cell layers of zinc-deficient group than those of the control group. TUNEL-positive cells were significantly more detected in the CA1 and CA3 pyramidal cell layers of zinc-deficient group. These results demonstrate that kainate-induced hippocampal cell death occurs more easily in zinc deficiency. Extracellular zinc concentration detected with ZnAF-2 was significantly decreased in the hippocampal CA3 of zinc-deficient mice, in agreement with the previous data measured by in vivo microdialsysis. Synaptically released zinc may be less involved in kainate-induced hippocampal cell death in zinc deficiency.     

Attenuation of abnormal glutamate release in zinc deficiency by zinc and Yokukansan

The mechanism of the abnormal increase in extracellular glutamate concentration in the hippocampus induced with 100 mM KCl in zinc deficiency is unknown. In the present study, the changes in glutamate release (exocytosis) and GLT-1, a glial glutamate transporter, expression were studied in young rats fed a zinc-deficient diet for 4 weeks. Exocytosis at mossy fiber boutons was enhanced as reported previously and GLT-1 protein was increased in the hippocampus. The enhanced exocytosis is thought to increase extracellular glutamate concentration. However, the basal concentration of extracellular glutamate in the hippocampus was not increased by zinc deficiency, suggesting that GLT-1 protein increased serves to maintain the basal concentration of extracellular glutamate. The enhanced exocytosis was attenuated in the presence of 100 μM ZnCl₂, which attenuated the abnormal increase in extracellular glutamate induced with high K⁺ in zinc deficiency. The present study indicates that zinc attenuates abnormal glutamate release in zinc deficiency. The enhanced exocytosis was also attenuated in slices from zinc-deficient rats administered Yokukansan, a herbal medicine, in which the abnormal increase in extracellular glutamate induced with high K⁺ was attenuated. It is likely that Yokukansan is useful for prevention or cure of abnormal glutamate release. The enhanced exocytosis in zinc deficiency is a possible mechanism on abnormal increase in extracellular glutamate in the hippocampus induced with high K⁺.     

缺磷条件下的小麦根系酸性磷酸酶活性研究

1　引　　言植物根可向根际分泌许多有机化合物 ,其中有许多物质都能促进植物对矿质养分的吸收 .作为必需大量营养元素的Ｐ ,在土壤中以无机磷酸盐阴离子的形式被吸收 ,而有机磷酸酯必须被水解成无机Ｐ后才能进入植物根 ,在这一过程中有一非常重要的步骤 ,就是由微生物、菌根外真菌和植物根分泌酸性磷酸酶 .土壤中的有机Ｐ一般占全Ｐ的 30 %～ 5 0 % ,有的可达95 % .因此 ,如何发挥植物自身利用土壤有机Ｐ的潜力已成为目前植物营养学研究的热点之一 .Ｇｏｌｄｓｔｅｉｎ等[3 ] 研究Ｐ胁迫条件下悬浮培养细胞时发现 ,抑制植物生长和诱导酸性…     

环境条件对不同品种小麦缺Mn的影响

在温室和网室中进行盆栽试验 ,研究不同环境条件和杂草对冬小麦缺Mn的影响 ,同时探讨不同小麦品种对缺Mn的耐性 ,发现生长在温室中的小麦其缺Mn症尤为严重 ,而从网室转移到温室的小麦因苗期在网室中受降雨渍水影响吸收了较多Mn2 ,缺Mn症就较轻 ,表明环境因子中降雨是影响小麦Mn营养的一个重要因素 ;供试的 3个品种中 331 7较耐缺Mn ,其Mn的吸收量明显高于敏感品种 .此外 ,试验还发现与小麦伴生的杂草麦麦草对Mn吸收能力强 ,是小麦根际Mn营养的有力争夺者 .     

土壤施Mn深度对不同基因型小麦缺Mn的影响

以缺Mn土壤为基质进行的小麦模拟土柱试验结果表明,不同施Mn深度条件下3317和川麦222个小麦基因型的缺Mn症、产量、根系分布和体内Mn含量均存在着显着差异。随着施Mn深度的增加,Mn肥的增产效果更为明显,川麦22施Mn的增产幅度高于3317.初步认为,3317耐缺Mn能力高于川麦22,与其根系在中下部土层分布比例高,吸Mn能力强有关。土柱试验发现小麦苗期的缺Mn症在中下部土层供Mn时明显恢复,表明中后期供Mn对小麦产量的形成有至关重要的作用.