Microbial Diversity and Biogeochemistry of a Shallow Pristine Canadian Shield Groundwater System

An investigation was conducted to assess the microbial diversity and biogeochemistry of a pristine shallow glaciofluvial groundwater system on the Canadian Shield. Vadose zone sands were very fine-grained, consisting mostly of iron oxide-coated quartz. Below the water table in the saturated zone, iron oxide-coating on quartz grains were absent, owing presumably to reductive dissolution by Fe(III)-reducing bacteria and chemical weathering, respectively. Groundwater pH was circumneutral at 6.4 + 0.1, and Eh was slightly reducing at 349 ± 15 mV compared to local surface waters at 417 ± 21 mV; the total dissolved solids concentration in groundwater was 45.2 ± 6.9 mg/L. A total of 269 clones were sequenced and compiled into a 16S rRNA gene library, and representative operational taxonomic units (OTU) were retrieved from basic local alignment search tool (BLAST) analyses at the species-level across 7 phyla, including Acidobacteria, Actinobacteria, Bacteroidetes, Chlorobi, Firmicutes, Planctomycetes, and Proteobacteria. Aerobic, anaerobic, and facultative anaerobic heterotrophs were predominant among the OTU. Lithoautotrophic ammonium- and nitrite-oxidizers were especially prominent, as were diazotrophs, nitrate- and nitrite-reducers. Representative OTU also included Fe(II)-oxidizers and Fe(III)-reducers, whereas those associated with sulfur cycling were rare. These observations suggest that there is considerable potential for biogeochemical cycling of nitrogen and iron within shallow glaciofluvial groundwater systems on the Canadian Shield.     

Iron and the heart: A paradigm shift from systemic to cardiomyocyte abnormalities

Iron is a key micronutrient for the human body and participates in biological processes, such as oxygen transport, storage, and utilization. Iron homeostasis plays a crucial role in the function of the heart and both iron deficiency and iron overload are harmful to the heart, which is partly mediated by increased oxidative stress. Iron enters the cardiomyocyte through the classic pathway, by binding to the transferrin 1 receptor (TfR1), but also through other routes: T-type calcium channel (TTCC), divalent metal transporter 1 (DMT1), L-type calcium channel (LTCC), Zrt-, Irt-like Proteins (ZIP) 8 and 14. Only one protein, ferroportin (FPN), extrudes iron from cardiomyocytes. Intracellular iron is utilized, stored bound to cytoplasmic ferritin or imported by mitochondria. This cardiomyocyte iron homeostasis is controlled by iron regulatory proteins (IRP). When the cellular iron level is low, expression of IRPs increases and they reduce expression of FPN, inhibiting iron efflux, reduce ferritin expression, inhibiting iron storage and augment expression of TfR1, increasing cellular iron availability. Such cellular iron homeostasis explains why the heart is very susceptible to iron overload: while cardiomyocytes possess redundant iron importing mechanisms, they are equipped with only one iron exporting protein, ferroportin. Furthermore, abnormalities of iron homeostasis have been found in heart failure and coronary artery disease, however, no clear picture is emerging yet in this area. If we better understand iron homeostasis in the cardiomyocyte, we may be able to develop better therapies for a variety of heart diseases to which abnormalities of iron homeostasis may contribute.     

Accumulation cyclique de fer et de quelques autres éléments dans le testicule de Littorina littorea (L.) (Gastéropode Prosobranche)

Iron, the presence of which can be revealed by histochemical techniques and microanalysis X, accumulates in the testis of Littorina littorea (L.). Its accumulation varies in relation to the annual cycle. The highest concentration occurs during the involution period (late summer) and is lowest during gametogenesis (early winter). Besides iron, S, P, Ca, Cl and sometimes Mg and F are found. These elements are contained in lysosomes of “epithelial cells” which develop in the testis following the reproductive stage.     

Effects of citrinin on iron-redox cycle

The ability of the mycotoxin citrinin to act as an inhibitor of iron-induced lipoperoxidation of biological membranes prompted us to determine whether it could act as an iron chelating agent, interfering with iron redox reactions or acting as a free radical scavenger. The addition of Fe3+ to citrinin rapidly produced a chromogen, indicating the formation of citrinin-Fe3+ complexes. An EPR study confirms that citrinin acts as a ligand of Fe3+, the complexation depending on the [Fe3+]:[citrinin] ratios. Effects of citrinin on the iron redox cycle were evaluated by oxygen consumption or the o-phenanthroline test. No effect on EDTA-Fe2+-->EDTA-Fe3+ oxidation was observed in the presence of citrinin, but the mycotoxin inhibited, in a dose-dependent manner, the oxidation of Fe2+ to Fe3+ by hydrogen peroxide. Reducing agents such as ascorbic acid and DTT reduced the Fe3+-citrinin complex, but DTT did not cause reduction of Fe3+-EDTA, indicating that the redox potentials of Fe3+-citrinin and Fe3+-EDTA are not the same. The Fe2+ formed from the reduction of Fe3+-citrinin by reducing agents was not rapidly reoxidized to Fe3+ by atmospheric oxygen. Citrinin has no radical scavenger ability as demonstrated by the absence of DPPH reduction. However, a reaction between citrinin and hydrogen peroxide was observed by UV spectrum changes of citrinin after incubation with hydrogen peroxide. It was also observed that citrinin did not induce direct or reductive mobilization of iron from ferritin. These results indicate that the protective effect on iron-induced lipid peroxidation by citrinin occurs due to the formation of a redox inactive Fe3+-citrinin complex, as well as from the reaction of citrinin and hydrogen peroxide.     

铁施肥促进海洋浮游植物和生物碳泵的不确定性

铁作为浮游植物所必需的微量元素,限制了全球超过三分之一海域的初级生产力,尤其是在高营养盐、低叶绿素海域(high nutrient low chlorophyll,HNLC)。长期以来海洋铁施肥被认为是一项可以降低大气二氧化碳含量的地球工程策略。然而通过13次海洋人工铁施肥(artificial ocean iron fertilization,aOIF)实验发现,铁的额外添加对海洋深层碳输出量的促进作用要显著低于预期。本文简要地总结了碳在海洋和大气中的循环过程,回顾了人工铁施肥实验对生物碳泵和碳通量等的影响,分析了从海洋铁施肥到海洋碳汇关键生物地球化学过程的影响因素。综上分析发现,科学界对生物碳泵过程及其调控机制的认识仍十分浅薄,考虑到海洋铁施肥还会对海洋生态系统带来一定的负面作用,铁施肥能否作为降低大气中CO₂的有效手段,以达到碳中和并缓解温室效应仍需进一步研究。     

Dynamics of Redox Changes of Iron Caused by Light–dark Variations in Littoral Sediment of a Freshwater Lake

Depth profiles of oxygen concentration and the redox status of acid-extractable iron were measured in littoral sediment cores of Lake Constance incubated under a light–dark regimen of 12 h. While oxygen penetrated to 3.4±0.2 mm depth in the dark, photosynthetic oxygen production shifted the oxic–anoxic interface down to 4.0±0.2 mm or 5.9±1.6 mm depth, at low or high light intensity, respectively, and caused a net oxygen efflux into the water column. After a light–dark or dark–light transition, the oxygen concentration at the sediment surface reached a new steady state within about 20 min. The redox state of the bioavailable iron was determined in 1-mm slices of sediment subcores. After a dark period of 12 h, 85% of the acid-extractable iron (10.5 μmol cm⁻³ total) in the uppermost 8 mm was in the reduced state. Within 12 h at low or high light intensity, the proportion of ferrous iron decreased to 82 or 75%, respectively, corresponding to net rates of iron oxidation in the range of 244 and 732 nmol cm⁻³ h⁻¹, respectively. About 55 or 82% of the iron oxidation at low or high light intensity occurred in the respective oxic zone of the sediment; the remaining part was oxidized in the anoxic zone, probably coupled to nitrate reduction. The areal rates of iron oxidation in the respective oxic layer (21 or 123 nmol cm⁻² h⁻¹ at low or high light intensity, respectively) would account for 4 and 23% of the total electron flow to oxygen, respectively. Light changes caused a rapid migration of the oxic–anoxic interface in the sediment, followed by a slow redox reaction of biologically available iron, thus providing temporal niches for aerobic iron oxidizers and anaerobic iron reducers.     

Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat

Managanese (Mn) is an essential trace element at low concentrations, but at higher concentrations is neurotoxic. It has several chemical and biochemical properties similar to iron (Fe), and there is evidence of metabolic interaction between the two metals, particularly at the level of absorption from the intestine. The aim of this investigation was to determine whether Mn and Fe interact during the processes involved in uptake from the plasma by the brain and other organs of the rat. Dams were fed control (70 mg Fe/kg), Fe-deficient (5–10 mg Fe/kg), or Fe-loaded (20 g carbonyl Fe/kg) diets, with or without Mn-loaded drinking water (2 g Mn/L), from day 18–19 of pregnancy, and, after weaning the young rats, were continued on the same dietary regimens. Measurements of brain, liver, and kidney Mn and nonheme Fe levels, and the uptake of⁵⁴Mn and⁵⁹Fe from the plasma by these organs and the femurs, were made when the rats were aged 15 and 63 d. Organ nonheme Fe levels were much higher than Mn levels, and in the liver and kidney increased much more with Fe loading than did Mn levels with Mn loading. However, in the brain the increases were greater for Mn. Both Fe depletion and loading led to increased brain Mn concentrations in the 15-d/rats, while Fe loading also had this effect at 63 d. Mn loading did not have significant effects on the nonheme Fe concentrations.⁵⁴Mn, injected as MnCl₂ mixed with serum, was cleared more rapidly from the circulation than was⁵⁹Fe, injected in the form of diferric transferrin. In the 15-d-rats, the uptake of⁵⁴Mn by brain, liver, kidneys, and femurs was increased by Fe loading, but this was not seen in the 63-d rats. Mn supplementation led to increased⁵⁹Fe uptake by the brain, liver, and kidneys of the rats fed the control and Fe-deficient diets, but not in the Fe-loaded rats. It is concluded that Mn and Fe interact during transfer from the plasma to the brain and other organs and that this interaction is synergistic rather than competitive in nature. Hence, excessive intake of Fe plus Mn may accentuate the risk of tissue damage caused by one metal alone, particularly in the brain.     

铁代谢蛋白在肾脏的表达与功能

最近的研究证实,肾小管细胞具有能力表达包括转铁蛋白受体1(transferrin receptor-1,TfR1)、二价金属离子转运蛋白1(divalent metal transporter-1,DMT1)、膜铁转运蛋白1(ferroportin-1,FPN1)、铁调节蛋白(iron regulatory protein,IRP)和铁调素(hepcidin,Hepc)在内的几乎所有铁代谢蛋白.这些蛋白质的存在以及相关研究显示肾脏可能具有排出多余铁的功能,因此对体铁平衡起有十分重要的作用.     

Iron oxidation stimulates organic matter decomposition in humid tropical forest soils

Humid tropical forests have the fastest rates of organic matter decomposition globally, which often coincide with fluctuating oxygen (O₂) availability in surface soils. Microbial iron (Fe) reduction generates reduced iron [Fe(II)] under anaerobic conditions, which oxidizes to Fe(III) under subsequent aerobic conditions. We demonstrate that Fe (II) oxidation stimulates organic matter decomposition via two mechanisms: (i) organic matter oxidation, likely driven by reactive oxygen species; and (ii) increased dissolved organic carbon (DOC) availability, likely driven by acidification. Phenol oxidative activity increased linearly with Fe(II) concentrations (P < 0.0001, pseudo R² = 0.79) in soils sampled within and among five tropical forest sites. A similar pattern occurred in the absence of soil, suggesting an abiotic driver of this reaction. No phenol oxidative activity occurred in soils under anaerobic conditions, implying the importance of oxidants such as O₂ or hydrogen peroxide (H₂O₂) in addition to Fe(II). Reactions between Fe(II) and H₂O₂ generate hydroxyl radical, a strong nonselective oxidant of organic compounds. We found increasing consumption of H₂O₂ as soil Fe(II) concentrations increased, suggesting that reactive oxygen species produced by Fe(II) oxidation explained variation in phenol oxidative activity among samples. Amending soils with Fe(II) at field concentrations stimulated short‐term C mineralization by up to 270%, likely via a second mechanism. Oxidation of Fe(II) drove a decrease in pH and a monotonic increase in DOC; a decline of two pH units doubled DOC, likely stimulating microbial respiration. We obtained similar results by manipulating soil acidity independently of Fe(II), implying that Fe(II) oxidation affected C substrate availability via pH fluctuations, in addition to producing reactive oxygen species. Iron oxidation coupled to organic matter decomposition contributes to rapid rates of C cycling across humid tropical forests in spite of periodic O₂ limitation, and may help explain the rapid turnover of complex C molecules in these soils.     

Calcein as a fluorescent iron chemosensor for the determination of low molecular weight iron in biological fluids

The fluorescence quenching of calcein (CA) is not iron specific and results in a negative calibration curve. In the present study, deferoxamine (DFO), a strong iron chelator, was used to regenerate the fluorescence quenched by iron. Therefore, the differences in fluorescence reading of the same sample with or without addition of DFO are positively and specifically proportional to the amounts of iron. We found that the same iron species but different anions (e.g. ferric sulfate or ferric citrate) differed in CA fluorescence quenching, so did the same anions but different iron (e.g. ferrous or ferric sulfates). Excessive amounts of citrate competed with CA for iron and citrate could be removed by barium precipitation. After optimizing the experimental conditions, the sensitivity of the fluorescent CA assay is 0.02 M of iron, at least 10 times more sensitive than the colorimetric assays. Sera from 6 healthy subjects were tested for low molecular weight (LMW) chelator bound iron in the filtrates of 10 kDa nominal molecular weight limit (NMWL). The LMW iron was marginally detectable in the normal sera. However, increased levels of LMW iron were obtained at higher transferrin (Tf) saturation (1.64–2.54 M range at 80% Tf saturation, 2.77–3.15 M range at 100% Tf saturation and 3.09–3.39 M range at 120% Tf saturation). The application of the assay was further demonstrated in the filtrates of human liver HepG2 and human lung epithelial A549 cells treated with iron or iron-containing dusts.     

过氧化氢加重铁对心肌的损伤作用及其机制

采用Langendorff灌流心脏和酶解分离的心肌细胞为实验模型,研究铁对心肌的损伤作用,以及过氧化氢对铁的心肌作用的影响及其可能机制.结果显示(1)羟基喹啉铁复合物(Fe-HQ)引起分离心肌细胞舒张期缩短,心肌细胞的收缩幅度和速度降低,离体灌流心脏左室发展压(LVDP)、±dp/dtmax、心率、冠脉流量呈现双相变化;冠脉流出液中乳酸脱氢酶(LDH)、肌酸激酶(CK)释放量和心肌丙二醛(MDA)增高.(2)H2O2可加重Fe-HQ对心脏的损伤,冠脉流出液中LDH、CK释放量和心肌MDA增高,而LVDP、±dp/dtmax和心率明显降低.(3)还原型谷胱甘肽可对抗Fe-HQ+H2O2对心肌的损伤作用,DMSO对Fe-HQ+H2O2致离体心脏损伤无明显作用.结果提示,心肌细胞内铁增加可引起心肌功能受损,H2O2可加重铁对心肌的损伤作用,其主要机制可能与@OH无关,而主要与含巯基的蛋白质受损有关.     

妊娠期糖尿病患者体内铁负荷状态及氧化应激水平的研究

为了探讨铁代谢在妊娠期糖尿病(GDM)发病中的作用,对GDM患者体内铁负荷状态、氧化应激水平及抗氧化状态进行分析研究.在912例孕24～28周产前检查的孕妇中,按血糖筛查和糖耐量试验筛选出GDM孕妇32例为实验组,随机选择糖耐量正常孕妇26例作为对照组,分别测定两组孕妇的血红蛋白(Hb)等指标,以评价机体铁代谢状况;测...     

Quiescence induced by iron challenge protects neuroblastoma cells from oxidative stress

The brain uses massive amounts of oxygen, generating large quantities of reactive oxygen species (ROS). Because of its lipid composition, rich in unsaturated fatty acids, the brain is especially vulnerable to ROS. Furthermore, oxidative damage in the brain is often associated with iron, which has pro-oxidative properties. Iron-mediated oxidative damage in the brain is compounded by the fact that brain iron distribution is non-uniform, being particularly high in areas sensitive to neurodegeneration. This work was aimed to further our understanding of the cellular mechanisms by which SHSY5Y neuroblastoma cells adapt to, and survive increasing iron loads. Using an iron accumulation protocol that kills about 50% of the cell population, we found by cell sorting analysis that the SHSY5Y sub-population that survived the iron loading arrested in the G(0) phase of the cell cycle. These cells expressed neuronal markers, while their electrical properties remained largely unaltered. These results suggest that upon iron challenge, neuroblastoma cells respond by entering the G(0) phase, somehow rendering them resistant to oxidative stress. A similar physiological condition might be involved in neuronal survival in tissues known to accumulate iron with age, such as the hippocampus and the substantia nigra pars compacta.     

Iron deficiency-induced changes in the photosynthetic pigment composition of field-grown pear (Pyrus communis L) leaves

In this work we characterize the changes induced by iron deficiency in the pigment composition of pear (Pyrus communis L.) leaves grown under high light intensities in field conditions in Spain. Iron deficiency induced decreases in neoxanthin and β-carotene concomitantly with decreases in chlorophyll a, whereas lutein and carotenoids within the xanthophyll cycle were less affected. Iron deficiency caused major increases in the lutein/chlorophyll a and xanthophyll cycle pigments/chlorophyll a molar ratios. The chlorophyll a/chlorophyll b ratio increased in response to iron deficiency. The carotenoids within the xanthophyll cycle in iron-deficient and in iron-sufficient (control) leaves underwent epoxidations and de-epoxidations in response to ambient light conditions. In control leaves dark-adapted for several hours, most of the xanthophyll cycle pigment pool was in the epoxidated form vio-laxanthin, whereas iron-deficient leaves had significant amounts of zeaxanthin. Iron-deficient leaves also exhibited an increased non-photochemical quenching, supporting the possibility of a role for pigments within the xanthophyll cycle in photoprotection.     

Liver iron depletion and toxicity of the iron chelator Deferiprone (L, CP20) in the guinea pig

The use of the iron chelator deferiprone (L, CP20, 1,2-dimethyl-3-hydroxypyrid-4-one) for the treatment of diseases of iron overload and other disorders is problematic and requires further evaluation. In this study the efficacy, toxicity and mechanism of action of orally administered L were investigated in the guinea pig using the carbonyl iron model of iron overload. In an acute trial, depletion of liver non-heme iron in drug-treated guinea pigs (normal iron status) was maximal (approximately 50% of control) after a single oral dose of L1 of 200 mg kg, suggesting a limited chelatable pool in normal tissue. There was no apparent toxicity up to 600 mg kg. In each of two sub-acute trials, normal and iron-loaded animals were fed L (300 mg kg day) or placebo for six days. Final mortalities were 12/20 (L) and 0/20 (placebo). Symptoms included weakness, weight loss and eye discharge. Iron-loaded as well as normal guinea pigs were affected, indicating that at this drug level iron loading was not protective. In a chronic trial guinea pigs received L (50 mg kg day) or placebo for six days per week over eight months. Liver non-heme iron was reduced in animals iron-loaded prior to the trial. The increase in a wave latency (electroretinogram), the foci of hepatic, myocardial and musculo-skeletal necrosis, and the decrease in white blood cells in the drug-treated/normal diet group even at the low dose of 50 mg kg day suggests that L may be unsuitable for the treatment of diseases which do not involve Fe overload. However, the low level of pathology in animals treated with iron prior to the trial suggests that even a small degree of iron overload (two-fold after eight months) is protective at this drug level. We conclude that the relationship between drug dose and iron status is critical in avoiding toxicity and must be monitored rigorously as cellular iron is depleted.     

Sex Accessories Morphology and Functions during the Seasonal Testicular Cycle of a Subtropical Wild Avian Species,the Yellow-Throated Sparrow Petronia xanthocollis Burton

Annual changes in the male sex accessories (tubuli recti, rete testis, vasa efferentia, epididymis, vas deferens and seminal glomus) were studied during the annual testicular cycle of the yellow-throated sparrow (Petronia xanthocollis Burton). All the segments of genital tract and the seminal glomus became enlarged during the progressive phase (January to March), were maximally enlarged during breeding (April), began to decrease during regression (May and June) and became maximally regressed during the nonbreeding phase (July to December). But the sialic acid level of the seminal glomus increased to maximum already during the progressive phase, remained high during breeding and declined subsequently. The findings suggest that the male sex accessories functions vary distinctly with the annual testicular cycle presumably due to alterations in the testicular androgen production in the yellow-throated sparrow.     

Krebs Cycle Intermediates Modulate Thiobarbituric Acid Reactive Species (TBARS) Production in Rat Brain <Emphasis Type="Italic">In Vitro</Emphasis>

The aim of this study was to investigate the effect of Krebs cycle intermediates on basal and quinolinic acid (QA)- or iron-induced TBARS production in brain membranes. Oxaloacetate, citrate, succinate and malate reduced significantly the basal and QA-induced TBARS production. The potency for basal TBARS inhibition was in the order (IC₅₀ is given in parenthesis as mM) citrate (0.37) > oxaloacetate (1.33) = succinate (1.91) >> malate (12.74). -Ketoglutarate caused an increase in TBARS production without modifying the QA-induced TBARS production. Cyanide (CN^–) did not modify the basal or QA-induced TBARS production; however, CN^– abolished the antioxidant effects of succinate. QA-induced TBARS production was enhanced by iron ions, and abolished by desferrioxamine (DFO). The intermediates used in this study, except for -ketoglutarate, prevented iron-induced TBARS production. Oxaloacetate, citrate, -ketoglutarate and malate, but no succinate and QA, exhibited significantly iron-chelating properties. Only -ketoglutarate and oxaloacetate protected against hydrogen peroxide-induced deoxyribose degradation, while succinate and malate showed a modest effect against Fe²⁺/H₂O₂-induced deoxyribose degradation. Using heat-treated preparations citrate, malate and oxaloacetate protected against basal or QA-induced TBARS production, whereas -ketoglutarate induced TBARS production. Succinate did not offer protection against basal or QA-induced TBARS production. These results suggest that oxaloacetate, malate, succinate, and citrate are effective antioxidants against basal and iron or QA-induced TBARS production, while -ketoglutarate stimulates TBARS production. The mechanism through which Krebs cycle intermediates offer protection against TBARS production is distinct depending on the intermediate used. Thus, under pathological conditions such as ischemia, where citrate concentrations vary it can assume an important role as a modulator of oxidative stress associated with such situations.     

Metabolism of some amino acids in relation to the photorespiratory nitrogen cycle of pea leaves

¹⁵N-labelled (amino group) asparagine (Asn), glutamate (Glu), alanine (Ala), aspartate (Asp) and serine (Ser) were used to study the metabolic role and the participation of each compound in the photorespiratory N cycle ofPisum sativum L. leaves. Asparagine was utilised as a nitrogen source by either deamidation or transamination, Glu was converted to Gln through NH₃ assimilation and was a major amino donor for transamination, and Ala was utilised by transamination to a range of amino acids. Transamination also provided a pathway for Asp utilisation, although Asp was also used as a substrate for Asn synthesis. In the photorespiratory synthesis of glycine (Gly), Ser, Ala, Glu and Asn acted as sources of amino-N, contributing, in the order given, 38, 28, 23, and 7% of the N for glycine synthesis; Asp provided less than 4% of the amino-N in glycine. Calculations based on the incorporation of¹⁵N into Gly indicated that about 60% (Ser), 20% (Ala), 12% (Glu) and 11% (Asn) of the N metabolised from each amino acid was utilised in the photorespiratory nitrogen cycle.Abbreviations Ala alamine - Asn asparagine - Asp aspartate - Glu glutamate - MOA methoxylamine - Ser serine     

基于多源数据的黄土高原陆地水循环结构变化分析

近几十年间,黄土高原的水循环进程在人类活动与气候变化的影响下已产生了剧烈的变化。为加深对水循环结构变化的了解与认识,利用1982-2010年的降水、蒸散发、径流、土壤储水量和社会经济用水等数据,运用Mann-Kendall趋势检验和线性回归分析方法,对黄土高原的水量平衡进行评估,且细化了组成水循环的12种水文变量,并分析了水循环各分量的变化趋势及其结构的演化规律。由于网格化的社会经济用水数据（1982-2010年）对本研究产生了较大的时间限制,因此本文注重于探究这29年间黄土高原各水文变量的变化趋势及水循环结构的演化规律。结果表明：在自然系统中,蒸散发以1.97 mm/a的速率上升（P<0.01）,径流、降水和土壤储水量分别以1.01 mm/a（P<0.01）、0.77 mm/a和0.46 mm/a的速率下降。在社会系统中,社会经济用水以0.50 mm/a的速率上升,其中主要由于生活、制造业、发电和采矿用水分别以0.22、0.23、0.30 mm/a和0.01 mm/a的速率增加所导致。此外,灌溉和牲畜用水分别以0.25 mm/a（P<0.05）、0.01 mm/a（P<0.01）的速率减少。就水循环结构而言,多年平均蒸散发和社会经济用水占水循环的平均比例分别为80.95%、15.27%,并以每年0.16%、0.06%的速率逐渐升高。径流、土壤储水量的变化占水循环的平均比例分别为4.00%、-0.24%,并以每年0.24%（P<0.01）、0.02%的速率逐渐下降。随着社会经济的发展和人口的增加,区域水资源供需矛盾将进一步加剧,本研究对黄土高原水资源的科学调控与可持续利用有重要参考意义。