土壤有机碳分解温度敏感性的影响机制研究进展

土壤有机碳(SOC)分解的温度敏感性(Q₁₀)是估算土壤碳收支动态的重要指标，但其空间变异特征及影响因素仍有较大的不确定性。本研究主要从气候环境、空间地理格局、土壤理化性质、植被类型、微生物群落组成及功能、全球气候变化等方面对Q₁₀的影响进行综述，总结各因子对Q₁₀影响的一般规律，比较其在不同生态系统中的相对贡献。Q₁₀随温度和降水的增加而减少，随纬度和海拔的升高而增加。草原SOC分解的Q₁₀高于森林，针叶林和落叶林SOC分解的Q₁₀高于常绿阔叶林。土壤碳(C)质量与Q₁₀呈反比，但在有外源底物输入时，C质量假说并不总是有效，在低质量土壤中提高底物可利用性可显著提高Q₁₀。Q₁₀随土壤中r策略型微生物(变形菌门、子囊菌门)比例的增加而降低，随K策略型微生物(酸杆菌门、担子菌门)比例的增加而增加。大气CO₂浓度升高增加了Q₁₀,而大气氮沉降降低了Q<...     

覆膜与滴灌对河套灌区玉米花粒期叶片光合特征的影响

光合作用是作物生长发育和产量形成的基础,栽培方式和土壤含水量变化显著影响作物的光合作用.灌浆期和乳熟期是玉米花粒期2个重要阶段,是玉米籽粒形成和干物质积累的关键时期.通过大田试验研究了河套灌区不同覆膜方式与滴灌水平对不同生育时期玉米光合特征及产量的影响.结果表明: 灌浆期玉米叶片光合特征在不同处理下无显著差异,乳熟期净光合速率和蒸腾速率在半覆膜(B₂)和全覆膜(Q₂)滴灌水平2(350 mm)处理下均显著高于半覆膜(B₁)和全覆膜(Q₁)滴灌水平1(200 mm),并且B₁和Q₁处理下灌浆期叶片的净光合速率、蒸腾速率、水分利用效率及气孔导度等显著高于乳熟期.不同处理下灌浆期和乳熟期叶片的净光合速率、蒸腾速率,灌浆期的气孔导度以及乳熟期的水分利用效率等在日变化上存在着同步关系,均呈现出倒“U”型的日变化特征,而胞间CO₂浓度则呈现相反的变化趋势.逐步回归分析显示,光合有效辐射、大气温度和空气相对湿度等气象因子是影响玉米叶片光合特征的主要环境因子.此外,B₂和Q₂处理下玉米产量显著高于B₁和Q₁处理(分别增加了29.3%和50.9%),但B₁和Q₁处理间并无显著差异.这表明与覆膜方式相比,滴灌水平对干旱地区玉米产量的影响更大.     

不同培养温度下严重侵蚀红壤的有机碳矿化特征

研究侵蚀土壤有机质矿化及其温度敏感性(Q₁₀)对深入认识水土流失地区土壤有机碳动态变化具有重要意义。该文以福建省长汀县河田镇严重侵蚀区的裸露红壤为研究对象, 通过测定不同培养温度(10 ℃、20 ℃和30 ℃)下的土壤有机碳矿化速率、培养过程中微生物生物量碳(MBC)和可溶性有机碳(DOC)含量的变化, 探讨了温度对严重侵蚀红壤有机碳矿化特征的影响及其Q₁₀。结果表明: 温度对严重侵蚀红壤有机碳矿化具有显著影响, 温度越高土壤有机碳矿化速率和矿化率越高; 培养过程中土壤有机碳累积矿化量与MBC显著正相关, 与DOC极显著负相关, 说明微生物生物量和可利用碳含量显著影响土壤有机碳的矿化。尽管严重侵蚀红壤有机碳含量仅为1.54 g·kg^-1, 但培养180天的土壤有机碳的累积矿化率高达22.2%-33.3%, 表明侵蚀红壤有机碳容易被矿化。严重侵蚀红壤在10-20 ℃时的Q₁₀值为1.41, 20-30 ℃时Q₁₀值下降到1.06, 土壤有机碳质量低是导致Q₁₀值较低的重要原因, 而严重侵蚀区的红壤长期裸露使微生物对高温产生适应性是高温时Q₁₀值接近1的重要原因。因此, 在未来气候变暖的趋势下, 恢复植被覆盖对减少严重侵蚀红壤有机碳矿化损失具有重要意义。     

北方温带森林不同海拔梯度土壤碳矿化速率及酶动力学参数温度敏感性

采集长白山脉龙岗支脉老秃顶子南坡3个不同海拔梯度森林(岳桦林、针阔混交林、红松林)土壤,进行室内温度梯度培养试验,研究土壤碳矿化速率(C_min)和土壤β-1,4-葡萄糖苷酶(β_G)动力学参数及温度敏感性.结果表明： 海拔和温度对C_min均有显著影响,3种森林土壤C_min均随着培养温度升高而增加,且岳桦林土壤C_min最高.3种森林土壤碳矿化速率温度敏感性\[Q₁₀(C_min)\]大小为岳桦林>红松林>针阔混交林,但差异不显著.3种森林土壤β_G动力学参数最大反应速率(V_max)和米氏常数(K_m)均随培养温度升高而增加,V_max的温度敏感性\[Q₁₀(V_max)\]为1.78～1.90,K_m的温度敏感性\[Q₁₀(K_m)\]为1.79～2.00.岳桦林Q₁₀(V_max)/Q₁₀(K_m)值显著高于红松林和针阔混交林,表明高海拔岳桦林土壤有机碳水解酶动力学参数受温度升高影响最大.     

小兴安岭原始阔叶红松林与枫桦次生林土壤呼吸及其各组分特征的比较研究

原始阔叶红松林是我国温带典型的地带性顶极植被类型,枫桦次生林是其典型的次生林类型之一,对二者土壤呼吸及其各组分特征的研究有助于准确评价该地区的碳平衡。本研究主要测定了2013和2014年2个生长季原始阔叶红松林和枫桦次生林土壤呼吸（R_S）,并量化了土壤呼吸的各个组分（异养呼吸R_H和自养呼吸R_A）,与此同时测量了土壤10 cm处温度以及土壤含水率。研究结果表明,土壤呼吸及其各组分有着明显的季节变化特性,其大小的变化主要受温度的影响,土壤10 cm处的温度可以解释R_S 64%~70%、R_H 56%~65%、R_A 77%~79%的变异。对于温度的敏感性,原始阔叶红松林土壤呼吸Q₁₀值>枫桦次生林土壤呼吸Q₁₀值,而在单一林型中的比较,R_A Q₁₀值 > R_S Q₁₀值 > R_H Q₁₀值。此外,总体Q₁₀值随着季节有着明显的变化,且随着温度的升高有降低的趋势。原始阔叶红松林和枫桦次生林R_S年平均速率分别为3.92和4.06 μmol·m^-2·s^-1,R_H年平均速率分别为2.97和2.85 μmol·m^-2·s^-1,R_A年平均速率则分别为0.96和1.17 μmol·m^-2·s^-1。原始阔叶红松林土壤呼吸以及土壤土壤自养呼吸要稍低于枫桦次生林,而原始阔叶红松林异养呼吸则高于枫桦次生林异养呼吸,但差异不显著。原始阔叶红松林和枫桦次生林R_S平均年通量分别为942和971 g C·m^-2·a^-1,R_H年通量分别为709和677 g C·m^-2·a^-1,R_A年通量则分别为215和276 g C·m^-2·a^-1。原始阔叶红松林R_S年通量略高于枫桦次生林R_S年通量,但差异不显著。我们的实验结果表明,小兴安岭地区枫桦次生林正向演替的过程中,植被演替变化对土壤呼吸及各组分的影响并不明显,相较于环境因子温度和湿度要小的多。     

西双版纳热带季节雨林与橡胶林土壤呼吸的季节变化

采用挖壕沟法与红外气体分析法,研究了西双版纳热带季节雨林和人工橡胶林内土壤呼吸包括根系呼吸、异养呼吸的干湿季动态变化.结果表明：季节雨林内土壤呼吸和异养呼吸速率均显著大于橡胶林(P＜0.01),但根系呼吸差异不显著;土壤温湿度是呼吸速率变化的主要影响因子,季节雨林和橡胶林内土壤呼吸和异养呼吸速率均为雨季＞干热季＞雾凉季,但季节雨林内根系呼吸为雨季＞雾凉季＞干热季,而橡胶林内为雾凉季＞雨季＞干热季;季节雨林内根系呼吸对土壤呼吸的贡献率(29%)小于橡胶林(42%,P＜0.01),而季节雨林内异养呼吸对土壤呼吸的贡献率为71%、橡胶林为58%;当5 cm土壤温度在12 ℃～32 ℃范围内变化时,季节雨林内土壤呼吸及根系呼吸、异养呼吸的Q₁₀值均大于橡胶林,且异养呼吸的Q₁₀值最大而根系呼吸的Q₁₀值最小.     

马尾松和苦槠林根际土壤矿化和根系分解CO2释放的温度敏感性

以中亚热带马尾松林和苦槠林为对象,原位收集根际和非根际土壤、树木不同生态功能的根系,开展15 ℃、25 ℃、35 ℃和45 ℃恒温培养模拟试验,采用密闭气室碱液吸收法测定53 d内CO₂释放的动态变化.结果表明: 两种森林类型不同温度下土壤矿化CO₂释放速率的根际效应介于1.12～3.09,且培养前期高于培养后期;15 ℃下马尾松林和苦槠林差异不显著,25 ℃和35 ℃下前者低于后者,45 ℃下则相反.不同培养温度下两树种吸收根分解的CO₂释放速率均高于过渡根和贮存根,且马尾松均低于苦槠.两种森林类型CO₂释放的Q₁₀值均为土壤(1.21～1.83)显著高于根系(0.96～1.36).两种森林类型土壤矿化CO₂释放的Q₁₀值差异不显著,而马尾松根系分解CO₂释放的Q₁₀值高于苦槠.推断全球变暖导致的土壤矿化CO2释放的增量将远远高于根系分解,且马尾松林高于苦槠林;地带性顶极群落应对气候变化的抵抗力强于先锋树种群落.     

鄱阳湖苔草湿地非淹水期CO2释放特征

2009年9月至2010年4月非淹水期,在鄱阳湖南矶湿地国家级自然保护区,选择以灰化苔草为建群种的洲滩湿地,设置土壤-植物系统(TC)、剪除植物地上部分(TJ)2个试验处理（分别代表生态系统和土壤呼吸）,利用密闭箱-气相色谱法测定了非淹水期鄱阳湖苔草湿地CO₂释放通量.结果表明：苔草湿地生态系统呼吸与土壤呼吸均具有明显的季节变化模式,释放速率变化范围分别为89.57～1243.99和75.30～960.94mg CO₂·m^-2·h^-1,土壤呼吸占生态系统呼吸的比例为64%(39%～84%);土壤温度是苔草湿地CO₂通量的主要控制因子,可以解释呼吸速率80%以上的变异;生态系统呼吸与土壤呼吸的温度敏感性指数(Q₁₀)分别为3.31和2.75,且冬季的Q₁₀值明显高于春秋季节;土壤水分与CO₂释放速率之间未达到显著相关;非淹水期,鄱阳湖苔草湿地是大气CO₂的汇,其强度为1717.72 g C·m^-2.     

黄土高原丘陵沟壑区柠条和沙棘树干液流的变化特征

近年来为防治黄土高原水土流失,我国政府开展了一系列的植被恢复工作。了解造林植被水分利用策略,对于在干旱半干旱黄土高原地区开展有效的植被恢复至关重要。以黄土高原甘肃省定西市安家沟小流域为研究区,选取黄土高原大规模植树造林灌木柠条(Caragana korshinskii)和沙棘(Hippophae rhamnoides)为研究对象,利用包裹式液流计于2020年6—9月对柠条和沙棘树干和枝条的液流进行观测,研究柠条和沙棘树干液流密度的日内与年内变化,以及与环境要素的关系。结果表明,柠条与沙棘的液流密度日内变化规律与光合有效辐射(Q₀)、饱和水汽压差(D_z)变化趋势一致。液流密度对环境要素的响应不同,在8月份,柠条和沙棘液流密度受D_z、Q₀和气温(T_a)的影响较大,其中,D_z占主导地位。在其他月份,液流密度主要受D_z、Q₀的影响较大。当柠条与沙棘经历了长期干旱无雨的条件下,土壤含水量对树干液流的影响较大,D_z...     

温度对温带和亚热带森林土壤有机碳矿化速率及酶动力学参数的影响

研究了温度对长白山阔叶红松林、鼎湖山常绿阔叶林2个不同纬度的森林土壤有机碳矿化速率和酶动力学参数的影响.结果表明:土壤有机碳矿化速率(C_min)随着温度的增加而增加,长白山土壤C_min及其温度敏感性(Q_10(Cmin))显著高于鼎湖山土壤.长白山土壤β-1,4-葡萄糖苷酶(βG)和β-1,4-N-乙酰葡糖氨糖苷酶(NAG)的酶动力学参数潜在最大反应速率(V_max)和半饱和常数(K_m)高于鼎湖山土壤,但鼎湖山土壤的催化效率(V_max/K_m)高于长白山土壤,表明随着温度的升高,土壤βG和NAG的V_max和V_max/K_m增加,K_m降低,即酶与底物的结合程度增加.鼎湖山土壤βG的Q_10(Vmax)、Q_10(Km)高于长白山土壤,这与土壤Q_10(Cmin)结果不一致.增温对长白山和鼎湖山森林土壤有机碳矿化及酶动力学参数的影响机制不同,在土壤生物化学过程对增温响应的模型中应区别考虑.     

快速提取类球红细菌中辅酶Q10的方法研究

目的：建立一种从类球红细菌中快速分离纯化辅酶Q10的方法。方法：对影响超声提取辅酶Q10的各因素,包括提取试剂、超声频率、循环次数及工作时间的最佳条件进行正交试验,比较超声破碎法与碱醇皂化法提取辅酶Q10的差异。结果：在超声提取中,提取试剂和循环次数对辅酶Q10提取效果具有显著性影响;在超声频率0.5s、丙酮提取3min、循环3次的条件下提取的辅酶Q10的含量比碱醇皂化法提高了近6倍。结论：超声破碎法是一种简单、迅速、高效的提取辅酶Q10方法。     

酵母发酵生产辅酶Q10提取方法研究进展

辅酶Q10是存在于哺乳动物中,能与酶蛋白形成复合物以发挥酶学活性的有机小分子化合物,目前广泛应用于医药、日化、保健、食品等不同领域。辅酶Q10来源丰富,其中酵母是其工业生产的主要来源之一。广受关注的酵母发酵生产辅酶Q10的提取分离手段不断革新,产量不断增加,处理方式更加环保,应用日渐拓宽。本文就近年来国内外酵母发酵生产辅酶Q10的提取分离方法进行了综述,包括酵母菌种的类型与优化、辅酶Q10提取检测方法、工业生产放大工艺以及与产品质量相关的各个影响因素,并对酵母发酵生产辅酶Q10的前景进行了展望。     

Effect of dopaminergic neurotoxin MPTP/MPP+ on coenzyme Q content

Coenzyme Q10, an endogenous lipophilic antioxidant, plays an indispensable role in ATP synthesis. The therapeutic value of coenzyme Q10 in Parkinson's disease and other neurodegenerative disorders is still being tested and the preliminary results are promising. The 1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine (MPTP)-treated mouse is a valid and accepted animal model for Parkinson's disease. 1-methyl-4-phenylpyridinium (MPP(+)) is an active toxic metabolite of MPTP. MPP(+) and MPTP are known to induce oxidative stress and mitochondrial dysfunction. However, the effect of MPP(+) and MPTP on coenzyme Q is not clearly understood. The present study investigated the in vitro and in vivo effect of MPP(+) and MPTP on coenzyme Q content. Coenzyme Q content was measured using HPLC-UV detection methods. In the in vitro studies, MPP(+) (0-50 microM) was incubated with SH-SY5Y human neuroblastoma cells and NG-108-15 (mouse/rat, neuroblastomaxglioma hybrid) cells. MPP(+) concentration dependently increased coenzyme Q10 content in SH-SY5Y cells. In NG-108-15 cells, MPP(+) concentration dependently increased both coenzyme Q9 and Q10 content. In the in vivo study, mice were administered with MPTP (30 mg/kg, twice 16 h apart) and sacrificed one week after the last administration. Administration of MPTP to mice significantly increased coenzyme Q9 and coenzyme Q10 levels in the nigrostriatal tract. However, MPTP did not affect the coenzyme Q content in the cerebellum, cortex and pons. This study demonstrated that MPP(+)/MPTP significantly affected the coenzyme Q content in the SH-SY5Y and NG-108 cells and in the mouse nigrostriatal tract.     

Systematic evaluation of muscle coenzyme Q10 content in children with mitochondrial respiratory chain enzyme deficiencies

Coenzyme Q10 content, pathology evaluation, and electron transport chain (ETC) enzyme analysis were determined in muscle biopsy specimens of 82 children with suspected mitochondrial myopathy. Data were stratified into three groups: "probable" ETC defects, "possible" ETC defects, and disease controls. Muscle total, oxidized, and reduced coenzyme Q10 concentrations were significantly decreased in the probable defect group. Stepwise logistic regression indicated that only total coenzyme Q10 was significantly associated with probable ETC defect. Receiver operator characteristic (ROC) analysis suggested that total muscle coenzyme Q10 was the best predictor of an ETC complex abnormality. Determination of muscle coenzyme Q10 deficiency in children with suspected mitochondrial disease may facilitate diagnosis and encourage earlier supplementation of this agent.     

High-sensitive determination of coenzyme Q(10) in iodinate-beta-cyclodextrin medium by inclusion reaction and catalytic polarography

A novel polarographic method for the determination of coenzyme Q(10) in beta-cyclodextrin (beta-CD) and iodinate system is proposed. The stability of coenzyme Q(10) to light was improved by the formation of coenzyme Q(10)-beta-CD inclusion complex. In addition, the sensitivity for the determination of coenzyme Q(10) was enhanced by both the formation and the polarographic catalytic wave of the inclusion complex in the presence of iodinate. In 0.1 mol/L HAc-NaAc (pH 4.7)-5.0 x 10(-5) mol/L beta-CD-1.2 x 10(-3) mol/L potassium iodinate-ethanol/water (60:40, v/v) medium, coenzyme Q(10)-beta-CD inclusion complex yielded a sensitive association/parallel catalytic wave. The second-order derivative peak current of the catalytic wave was proportional to coenzyme Q(10) concentration in the range of 6.0 x 10(-8)-2.5 x 10(-7) mol/L, and the detection limit was 1.0 x 10(-8) mol/L. The proposed method has high analytical sensitivity and is allowed to determine coenzyme Q(10) under light.     

Essentiality of coenzyme Q for the oxidation of -glycerophosphate by pig brain mitochondria

Serial extraction of lyophilized pig brain mitochondria with cold pentane resulted in complete loss of α-glycerophosphate oxidase activity. On titration with coenzyme Q₁₀ the activity was fully recovered. On comparing the decline of α-glycerophosphate, NADH, and succinoxidase activities during serial extraction with pentane, α-glycerophosphate oxidation was always the first to be lost. Extraction of coenzyme Q₁₀ from lyophilized brain mitochondria with pentane does not affect the activities of α-glycerophosphate or NADH dehydrogenase, but succinate dehydrogenase is partially inactivated. Reversible inactivation of the α-glycerophosphate oxidase system on depletion of the coenzyme Q content is taken as evidence that coenzyme Q is an obligatory component of this system. In accord with the conclusion that coenzyme Q is probably the physiological oxidant of α-glycerophosphate dehydrogenase, in antimycin-treated brain mitochondria α-glycerophosphate causes full activation of endogenous succinate dehydrogenase, in analogy to the previously observed activation by NAD-linked substrates in liver and heart mitochondria and by NADH in submitochondrial particles.     

Protection of Rat Myocardium by Coenzyme Q during Oxidative Stress Induced by Hydrogen Peroxide

Ubiquinone Q(10) (coenzyme Q) is an important component of the mitochondrial electron transport chain and an antioxidant. The purpose of this work was to find out whether an increase in the level of coenzyme Q in the heart changes its maximal working capacity and resistance to oxidative stress. Male Wistar rats were treated with coenzyme Q (10 mg/kg body weight per day) for six weeks, and this increased its content in the myocardium by 63%. The myocardial content of malonic dialdehyde and activities of key antioxidant enzymes were unchanged, except nearly 2.5-fold decrease in the activity of superoxide dismutase. The maximal working capacity of the isolated isovolumic heart did not change, but under conditions of oxidative stress induced by 45-min infusion of hydrogen peroxide (70 micro M) into coronary vessels the contractile function of these hearts decreased significantly more slowly. This was associated with less pronounced lesions in the ultrastructure of cardiomyocytes and lesser disorders in the oxidative metabolism of mitochondria that suggested increased antioxidant protection of the myocardium.     

Redox state of glutathione and thioredoxin in differentiation and apoptosis

This study was organized by Professor Karl Folkers with the objective of finding derivatives of coenzyme Q which could be more effectively absorbed and would give better biomedical effects. In this series all the compounds are 2,3 dimethoxy, 5 methyl p benzoquinone with modified side chains in the 6 position. The modifications are primarily changes in chain length, unsaturation, methyl groups and addition of terminal phenyl groups. The test system evaluates the growth of serum deficient HL60, 3T3 and HeLa cells in the presence of coenzyme Q10 or coenzyme Q analogs. Short chain coenzyme Q homologues such as coenzyme Q2 give poor growth but compounds with saturated short aliphatic side chains from C10 to C18 produce good growth. Introduction of a single double bond at the 2' or 8' position in the aliphatic chain retains growth stimulation at low concentration but introduces inhibition at higher concentration. Introduction of a 3' methyl group in addition to the 2' enyl site in the side chain decreases the growth response and maintains inhibition. Addition of a terminal phenyl group to the side chain from C5 to C10 can produce analogs which give strong stimulation or strong inhibition of growth. The action of the analogs is in addition to the natural coenzyme Q in the cell and is not based on restoration of activity after depletion of normal coenzyme Q. The effects may be based on any of the sites in the cell where coenzyme Q functions. For example, coenzyme Q2 is known to decrease mitochondrial membrane potential whereas the analog with a 10C aliphatic side chain increases potential. Both of these compounds stimulate plasma membrane electron transport. Inhibition of apoptosis by coenzyme Q may also increase net cell proliferation and the 10C analog inhibits the permeability transition pore.     

Inhibition by coenzyme Q of ethanol- and carbon tetrachloride-stimulated lipid peroxidation in vivo and catalyzed by microsomal and mitochondrial systems

The ability of coenzyme Q to inhibit lipid peroxidation in intact animals as well as in mitochondrial, submitochondrial, and microsomal systems has been tested. Rats fed coenzyme Q prior to being treated with carbon tetrachloride or while being treated with ethanol excrete less thiobarbituric acid-reacting material in the urine than such rats not fed coenzyme Q. Liver homogenates, mitochondria, and microsomes isolated from rats treated with carbon tetrachloride and ethanol catalyze lipid peroxidation at rates which exceed those from animals also fed coenzyme Q. The rate of lipid peroxidation catalyzed by submitochondrial particles isolated from hearts of young, old, and endurance trained elderly rats was inversely proportional to the coenzyme Q content of the submitochondrial preparation in assays in which succinate was employed to reduce the endogenous coenzyme Q. Reduced, but not oxidized, coenzyme Q inhibited lipid peroxidation catalyzed by rat liver microsomal preparations. These results provide additional evidence in support of an antioxidant role for coenzyme Q.