锌酵母分批流加发酵动态优化

对锌酵母分批流加发酵过程的控制变量反应温度和pH的动态最优化进行研究。基于酵母流加发酵有抑制的状态模型．通过龙格一库塔法计算微分方程组、单纯形法优化对模型参数进行估计。采用不同的温度和pH控制策略进行研究,由此获得动力学模型参数与温度和pH关系的回归模型。在此基础上,以极大值原理、梯度法优化求解以获得最高锌酵母产量为目标的最优温度和pH分布T*（t）、pH*(t)。实验验证,在T*(t)和pH*(t)下操作,锌酵母产率可提高13.7％。     

酵母和植物的锌转运系统及其调控

锌是所有生物体必需的微量元素之一, 是多种蛋白的辅酶并参与催化生物体内的一些重要生化反应。生物体为了维持细胞内适当的锌浓度以保证其正常功能而进化出了复杂的锌转运及调控系统。本文主要论述酵母和植物中的锌转运系统及其调控, 以及锌吸收的分子标记和QTL位点分析。     

酵母和植物的锌转运系统及其调控

锌是所有生物体必需的微量元素之一,是多种蛋白的辅酶并参与催化生物体内的一些重要生化反应。生物体为了维持细胞内适当的锌浓度以保证其正常功能而进化出了复杂的锌转运及调控系统。本文主要论述酵母和植物中的锌转运系统及其调控,以及锌吸收的分子标记和QTL位点分析。     

高锌酵母的试验研究

以啤酒酵母（Ｓａｕｈａｒｏｍｙｃｅｓｃｅｒｅｖｉｓｉａｅ）２号为菌种,利用玉米糖化液加入适当的营养元素及锌离子,经发酵试验获得高锌酵母产品,细胞富锌量在５８８１．６ｐｐｍ,干酵母收率为１．４ｇ／１００ｍｌ。     

血锌与肝锌,骨骼锌及肌肉锌的相关性研究

用~(65)Zn同位素示踪法研究了不同年龄LACA小鼠体内血锌与肝脏锌、骨骼锌及肌肉锌的相关性。实验结果表明,血锌的代谢与骨骼内锌及肌肉内锌的代谢有明显的相关关系,而与肝脏内锌代谢无相关关系;骨骼及肌肉中锌含量占全身锌含量的90％,上述结果提示血锌的监测可反映体内锌的水平。     

用模式识别法优化微生物培养基的营养条件

应用模式识别方法,对微生物培养的营养条件进行优化。以培养基组成构筑模式空间,通过主成份分析（ＰＣＡ）揭示模式空间的可视优化区,建立模式分类器并道推回到高维空间得到最佳培养基组成。以锌酵母为例。介绍优化全过程。     

模式识别在锌酵母发酵工艺优化控制中的应用

发酵过程是一个复杂的多元体系。对其工艺条件优化和控制的数学定量化程度还较低。本文尝试将模糊集和模式识别的理论和方法引入发酵过程研究。以锌酵母发酵工艺条件优化为目的,获得了酵母产量高、糖转化率高及残糖浓度低等诸因素综合考虑的优化控制区。1 材料与方法     

锌缺乏小鼠血锌与肝锌,骨骼锌及肌肉锌的相关性研究

必需微量元素锌营养的研究是一个非常活跃的领域,而其中一个中心问题是如何确定体锌缺乏,目前指标多为血锌、血清碱性磷酸酶、临床体征等。对于血锌作为指标颇多争议。本实验室曾报道体锌正常时血锌的监测能够反映机体锌水平,那么体锌缺乏时呢? 本实验就此进行探讨。 1 材料和方法 动物分组、饲养和饲料配方见文献[2],动物处理、样品测量及统计分析方法见文献[1]。 2 结果 2.1 血锌与肝锌的相关分析 机体锌缺乏及正常小鼠     

锌酵母中酵母甘露多糖组分的特征和结构

本文研究从锌酵母中分离出的酵母甘露多糖ＸＰ的特征和结构。ＸＰ经全水解和＾１３ＣＮＭＲ谱显示除甘露糖基外,还有少量Ｌ－鼠李糖基和甲氧基。甲基化分析、过碘酸盐氧化、Ｓｍｉｔｈ降解、乙酰解和部分酸水解显示ＸＰ的主链是１→６连接的甘露糖,侧链是１→２连接的甘露糖。＾１Ｈ及＾１３Ｃ ＮＭＲ谱表明所有糖苷键均为α型,结合元素分析ＸＰ基本是酵母甘露多糖和蛋白质以及锌的络合物。     

金针菇富锌条件及锌结合形态的研究

对金针菇深层发酵富锌培养条件进行了研究,并对Zn的生物有机化程度进行了初步探讨。结果表明,金针菇富锌的深层培养较好的Zn源为ZnAc_2,初始pH值为6.5,加入0.1％柠檬酸和0.4％的CMC-Na利于富锌和提高生物量。金针菇富锌过程中,93％以上的ZnAc_2以有机锌态存在,其中50％以上结合为Zn-蛋白,34％与糖及脂肪类物质结合。     

Zinc Supplementation or Regulation of its Homeostasis: Advantages and Threats

To accomplish its multifunctional biological roles, zinc requires precise homeostatic mechanisms. There are efficient mechanisms that regulate zinc absorption from the alimentary tract and its excretion by the kidney depending on the organism demands. The regulatory mechanisms of cellular zinc inflow, distribution, and zinc outflow are so efficient that symptoms of zinc deficiency are rare, and symptoms connected with its massive accumulation are even more rare. The efficiency of homeostatic mechanisms that prevent zinc deficiency or excessive zinc accumulation in the organism is genetically conditioned. It seems that an essential element of zinc homeostasis is the efficiency of zinc transmembrane exchange mechanisms. Intracellular free zinc concentration is higher than in extracellular space. Physiologically, the active outflow of zinc ions from the cell depends on the increase of its concentration in extracellular space. The ion pumps activity depends on the efficiency by which the cell manages energy. Considering the fact that zinc deficiency accelerates apoptosis and that excessive zinc accumulation inside cells results in a toxic effect that forces its death brings about several questions: Is intensification and acceleration of changes in zinc metabolism with age meaningful? Is there a real zinc deficiency occurring with age or in connection with the aforementioned pathological processes, or is it just a case of tissue and cell redistribution? When discussing factors that influence zinc homeostasis, can we consider zinc supplementation or regulation of zinc balance in the area of its redistribution? To clarify these aspects, an essential element will also be the clear understanding of the nomenclature used to describe changes in zinc balance. Zinc homeostasis can be different in different age groups and depends on sex, thus zinc dyshomeostasisrefers to changes in its metabolism that deviate from the normal rates for a particular age group and sex. This concept is very ample and implies that zinc deficiency may result from a low-zinc diet, poor absorption, excessive loss of zinc, zinc redistribution in intra- and extracellular compartments, or a combination of these factors that is inadequate for the given age and sex group. Such factor or factors need to be considered for preventing particular homeostasis disorders (or dyshomeostasis). Regulation of zinc metabolism by influencing reversal of redistribution processes ought to be the main point of pharmacologic and nonpharmacologic actions to reestablish zinc homeostasis. Supplementation and chelation are of marginal importance and can be used to correct long-term dietary zinc deficiency or zinc poisoning or in some cases in therapeutic interventions. In view of its biological importance, the problem posed by the influence of zinc metabolism requires further investigation. To date, one cannot consider, for example, routine zinc supplementation in old age, because changes of metabolism with age are not necessarily a cause of zinc deficiency. Supplementation is warranted only in cases in which deficiency has been established unambiguously. An essential element is to prevent sudden changes in zinc metabolism, which lead to dyshomeostasis in the terms defined here. The primary prophylaxes, regular physical activity, efficient treatment of chronic diseases, are all elements of such prevention.     

人内皮抑素在毕赤酵母中的表达、纯化与生物功能研究

内皮抑素（Endostatin）是近年来新发现的一种内源性新生血管生成（Angiogenesis）抑制因子,通过抑制新血管生成而抑制肿瘤的形成和转移且不会引起耐药性,具有极高的临床应用前景。巴斯德毕赤酵母（Pichia pastoris)具有表达率高、产物可分泌、可对高等真核生物蛋白正确进行翻译后加工、遗传稳定、发酵工艺成熟等优点被用来进行重组人Endostatin的表达。本研究用PCR的方法从人胎肝cDNA文库中扩增出人Endostatin的cDNA,测序正确后转入毕赤巴斯德甲醇酵母,并获得了高效可溶型表达,用肝素亲和层析的方法进行纯化,纯化后产物经SDSPAGE薄层扫描分析纯度达987％以上,质谱测定分子量为2043kD与理论值一致,蛋白质N端序列测定结果为SPPAHTHRDFQPVLH与天然序列一致。生物活性检测证明可抑制鸡胚尿囊绒毛膜（CAM）的新生血管生成（Angiogenesis),并可抑制血管内皮细胞的增殖。因此用酵母表达系统可以得到具有生物活性的内皮抑素,经纯化后可用于进一步的生物功能和作用机理试验。     

Role of zinc in regulation of arterial blood pressure and in the etiopathogenesis of arterial hypertension

Increased gastrointestinal absorption and urinary excretion of zinc has been confirmed in experimental and clinical studies on primary arterial hypertension as a result from changes of intracellular and extracellular zinc content. In arterial hypertension, the levels of zinc in serum, lymphocyte, and bone decrease while increasing in heart, erythrocytes, kidney, liver, suprarenal glands and spleen. These changes result in the loss of zinc homeostasis that leads to various degrees of deficiency, not entirely compensated by nutritional factors or increased absorption in the gastrointestinal tract. Loss of zinc homeostasis can be both cause and effect of high blood pressure. In the present review, the role of zinc metabolism changes and its mechanisms in arterial hypertension are discussed.     

Interplay Between Autophagy and Zinc

Autophagy is a conserved catabolic process that plays an important role in cellular homeostasis. The study of the interplay between autophagy and zinc has gained interest over the last years. Multiple studies have indicated that zinc stimulates autophagy and is critical for basal and induced autophagy in mammalian cells. Conversely, autophagy is induced by zinc starvation in yeast. There are no studies analyzing the role of zinc in either Microautophagy or Chaperone-Mediated-Autophagy. The mechanisms by which zinc modulates autophagy are still poorly understood. Studies examining loss of function of genes involved in cellular zinc homeostasis have provided novel insights into the role of zinc in autophagy. Autophagy may help cells adapt to changes in zinc availability in medium by controlling zinc mobilization, recycling, and secretion. Zinc is a key player in toxic and protective autophagy.     

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.     

Histidine residues in the region between transmembrane domains III and IV of hZip1 are required for zinc transport across the plasma membrane in PC-3 cells

The proteins from the ZIP and the CDF families of zinc transporters contain a histidine-rich sequence in a loop domain located between transmembrane domains III and IV for the ZIP family and transmembrane domains IV and V for the CDF family. Topological predictions suggest that these loops are located in the cytoplasm. The loops contain a histidine-rich sequence with a variable number of histidine residues depending on the transporter. The histidine-rich sequence was postulated to serve as an extra-membrane metal binding site in these proteins. hZip1 is a human zinc transporter ubiquitously expressed. The histidine-rich motif located in the large loop of this transporter is composed of the following sequence, H₁₅₈WHD₁₆₁. To determine if this motif is involved in the zinc transport activity of the protein, we performed site directed-mutagenesis to replace the loop histidines with alanines. Results suggest that both histidines are necessary for the zinc transport function and are not involved in the plasma membrane localization of the transporter as has been reported for the Zrt1 transporter in yeast. In addition, two histidine residues in transmembrane domains IV and V are also important in the zinc transport function. The results support an intermolecular exchange mechanism of zinc transport.     

MTM1 plays an important role in the regulation of zinc tolerance in Saccharomyces cerevisiae

BackgroundAcquisition and distribution of zinc supports a number of biological processes. Various molecular factors are involved in zinc metabolism but not fully explored.Basic proceduresSpontaneous mutants were generated in yeast with excess zinc culture followed by whole genome DNA sequencing to discover zinc metabolism related genes by bioinformatics. An identified mutant was characterized through metallomic and molecular biology methods.Main findingsHere we reported that MTM1 knockout cells displayed much stronger zinc tolerance than wild type cells on SC medium when exposed to excess zinc. Zn accumulation of mtm1Δ cells was dramatically decreased compared to wild type cells under excessive zinc condition due to MTM1 deletion reduced zinc uptake. ZRC1 mRNA level of mtm1Δ cells was significantly higher than that in the wild-type strain leading to increased vacuolar zinc accumulations in mtm1Δ cells. The mRNA levels of ZRT1 and ZAP1 decreased in mtm1Δ cells contributing to less Zn uptake. The zrc1Δmtm1Δ double knockout strain exhibited Zn sensitivity. MTM1 knockout did not afford resistance to excess zinc through an effect mediated through an influence on levels of ROS. Superoxide dismutase 2 (Sod2p) activity in mtm1Δ cells was severely impaired and not restored through Zn supplementation. Meanwhile, additional Zn showed no significant effect on the localization and expression of Mtm1p.Principal conclusionsOur study reveals the MTM1 gene plays an important role in the regulation of zinc homeostasis in yeast cells via changing zinc uptake and distribution. This discovery provides new insights for better understanding biochemical communication between vacuole and mitochondrial in relation to zinc-metabolism.     

Ydj1p锌指结构突变体对底物结合影响的分子动力学模拟分析

Ydj1p是酵母细胞质中一种主要的I型Hsp40分子伴侣,Ydj1p锌指结构在传递底物给Hsp70时发挥重要的作用,锌指结构域的两个锌离子结合位点区域(ZBDⅠ和ZBDⅡ)与半胱氨酸形成配位键对底物传递中维持结构稳定非常重要。本研究通过分子动力学手段对Ydj1p与各锌指结构突变体进行了模拟,分析ZBDⅠ突变体关键残基C143S、C201S,ZBDⅡ突变体关键残基C162S、C185S的突变影响Hsp40与Hsp70的底物传递。分析结果表明,当锌指部位的氨基酸发生突变,不仅能影响Ydj1p的结构稳定性,也能影响底物的传递,并且锌指结构Ⅰ突变体和锌指结构Ⅱ突变体之间也具有明显差异。通过结合能量的分析以及构象变化比对,揭示了Ydj1p以及各锌指结构突变体底物结合能力的强弱,这与生化实验研究了Ydj1p锌指结构与Hsp70合作,帮助多肽传递的功能是至关重要的结果较为相近。     

植物在渗透胁迫下的基因表达及信号传递

渗透胁迫是指由于环境因素的变化使植物不能得到充足水分的一种状况。常见的渗透胁迫因素有干旱、盐害及冻害等。渗透胁迫会严重影响植物的生长发育及产量。植物在长期的进化过程中形成了一些保护机制能减轻渗透胁迫造成的伤害。比如有些植物在形态上演化生成盐腺,能排出体内的过量盐分以逃避盐害。但在渗透胁迫下几乎所有的植物都能合成一些无毒性的小分子有机物作为渗透调节剂来维持细胞内渗透势的相对稳定。在分子水平上...     

Comparative Bioavailability of Mineral-enriched Gluconates and Yeast in Rat Liver After Depletion–Repletion Feeding

There are many forms of mineral supplements currently available. Among these mineral-enriched gluconates and yeast are considered two of the more biologically available supplements. The purpose of this study was to use zinc (Zn)- or copper (Cu)-deficient rats to determine whether the organically bound mineral in yeast or the salt gluconate form was more bioavailable, i.e., is absorbed and found in a greater concentration in liver. It was demonstrated that Zn-enriched yeast was 3.7 times more bioavailable than the Zn gluconate and that Cu-enriched yeast was 1.4 times more bioavailable than the Cu gluconate.