细根分解研究及其存在的问题

细根分解是陆地生态系统C和养分循环的重要环节.主要包括淋溶和破碎等物理过程和以生物作用为主的化学过程.这些过程受复杂的细根化学成分及外部土壤因子的综合控制,如细根本身养分含量、木质素和纤维素含量、土壤温度、水分、养分的有效性以及土壤动物、真菌和细菌等.但是,细根分解发生在不能直接观测的地下部分,人为改变细根分解的自然环境是研究过程中存在的主要问题.埋袋法虽然应用最为普遍,但是它严重地干扰了细根分解环境,导致低估分解速率.最近提出的原状土芯法(intact-core)克服了埋袋法的主要缺陷,是目前细根分解研究中最接近自然分解过程的研究方法,但也存在一些问题.因此,如何设计有效且能够真实的反映细根自然分解过程的试验方法是今后该领域研究最重要和最具挑战性的课题.     

细根分解研究及其存在的问题

细根分解是陆地生态系统C和养分循环的重要环节。主要包括淋溶和破碎等物理过程和以生物作用为主的化学过程。这些过程受复杂的细根化学成分及外部土壤因子的综合控制,如细根本身养分含量、木质素和纤维素含量、土壤温度、水分、养分的有效性以及土壤动物、真菌和细菌等。但是,细根分解发生在不能直接观测的地下部分,人为改变细根分解的自然环境是研究过程中存在的主要问题。埋袋法虽然应用最为普遍,但是它严重地干扰了细根分解环境,导致低估分解速率。最近提出的原状土芯法(intact-core)克服了埋袋法的主要缺陷,是目前细根分解研究中最接近自然分解过程的研究方法,但也存在一些问题。因此,如何设计有效且能够真实的反映细根自然分解过程的试验方法是今后该领域研究最重要和最具挑战性的课题。     

三峡库区马尾松不同直径细根分解动态及其影响因素

在三峡库区秭归县九岭头林场马尾松人工林进行一年的细根分解试验,研究马尾松直径<0.5、0.5～1和1～2 mm细根的分解动态及其影响因素.结果表明: 细根分解速率随直径增大而减小,直径<0.5、0.5～1和1～2 mm细根年分解率分别为34.0%、28.0% 和25.7%.直径<1 mm细根分解速率随时间增加而逐渐减小,直径1～2 mm细根分解速率随时间增加先逐渐增加再减小.在细根分解过程中,N、P和Ca浓度随时间增加而增加,K浓度呈先降低后上升再下降的趋势.细根分解速率与细根初始N、P、K和Ca浓度,以及C/N、C/P均显著相关,细根Ca浓度和土壤温度是影响细根分解的主导因子.     

林木细根寿命及其影响因子研究进展

 细根周转要消耗大量的C,它影响森林生态系统C分配格局与过程和养分循环,对生态系统生产力具有重要意义。细根的周转取决于细根的寿命,细根寿命越短,周转越快,根系对C的消耗也越多。大量研究表明,细根的寿命与地上部分C向根系供应的多少有密切关系,同时也与细根直径大小、土壤中N和水分的有效性、土壤温度以及根际周围的土壤动物和微生物的活动有关。本文综述了国外近年来在该领域里的研究进展,特别是对控制细根寿命的机理和主要影响因子进行了评述,目的是引起国内研究者的关注,促进我国根系生态学的研究与发展。     

华西雨屏区苦竹细根分解对模拟氮沉降的响应

森林细根分解是陆地生态系统碳循环的重要过程之一,其分解速率受到大气氮沉降增加的潜在影响.2007年11月至2013年1月,对华西雨屏区苦竹人工林进行每月1次的模拟氮沉降试验,设对照(CK,0 g N·m-2·a-1)、低氮(5 g N·m-2·a-1)、中氮(15 g N·m-2·a-1)和高氮(30 g N·m-2·a-1)4个处理.2011年1月起,采用分解袋法研究苦竹细根分解.结果表明:苦竹细根分解呈现出先快后慢的趋势,在分解第1年质量损失达60%,分解第2年质量残留率变化较为平缓.对照处理细根质量损失50%和95%分别需要1.20和5.17 a.总体上,负指数模型低估了各处理细根分解速率.模拟氮沉降显著抑制了苦竹细根分解,相对于对照,高氮处理细根在分解2 a后残留量增加51.0%.模拟氮沉降显著增加了凋落物碳、氮和磷元素的残留率.与对照相比,模拟氮沉降处理4.5 a后,中氮和高氮处理土壤pH值显著降低,高氮处理土壤有机碳、总氮、铵态氮和硝态氮含量以及苦竹细根生物量显著增加.     

不同营林措施对马尾松细根分解与养分释放的影响

细根(直径≤2 mm)是森林生态系统重要的碳库之一,其寿命短、代谢活性高,对外界环境变化十分敏感.了解不同营林措施对细根分解和养分释放的影响,对于合理开展森林经营管理具有重要意义.以三峡库区马尾松(Pinus massoniana)飞播林为对象,设置未择伐(NC)、除灌(SC)、伐除非马尾松(NPMC)和伐除优势马尾松(DPMC)等营林措施,在处理3年后,利用分解袋法研究不同营林措施对相同初始基质质量的马尾松细根分解和养分释放的影响.经过1年的分解,不同营林措施明显改变了土壤温湿度、土壤养分以及土壤微生物量碳氮,而对马尾松细根分解速率的影响不显著(P>0.05),细根分解速率与各环境因子间均无显著相关性.在分解过程中,各营林措施的细根C残留率逐渐降低,表现为DPMC>SC>NC>NPMC.N呈现先逐渐累积后释放的状态,P呈现释放-累积-释放的状态,且抚育择伐显著降低了P释放速率.短期来看,不同营林措施造成的林内环境因素变化不足以成为影响马尾松细根分解的主导因素,细根初始基质质量仍是影响细根分解的决定性因素.抚育择伐提高了细根C释放速率,降低了N和P元素的释放速率.     

树木细根生产与周转研究方法评述

树木细根在森林生态系统能量流动和物质循环中起重要的作用。树木细根研究及方法探讨也成为当今森林生态学的研究热点。在中国,对树木细根生产和周转的研究尚未引起充分重视。在此介绍了目前国外普遍采用的树木细根研究方法及其优缺点、适用性以及不同方法的研究比较,以期对我国开展树木细根方面的研究有所裨益。     

水曲柳和兴安落叶松人工林细根分解研究

  细根分解是陆地生态系统C和养分循环的重要环节。以往的细根分解研究以埋袋法的应用为主。然而, 由于埋袋法对分解材料的干扰以及对分解环境的改变使其很难揭示原位环境下根系的自然分解过程。该研究应用微根管(Minirhizotron)技术连续3年对水曲柳(Fraxinus mandshurica)和兴安落叶松(Larix gmelinii)细根的分解过程进行原位监测, 运用Kaplan–Meier方法估算细根分解的保存率及分解期中位值(即50%细根完全分解的时间, Median root decomposition time), 做分解曲线, 用对数秩检验(Log-rank test)方法分析不同树种、直径、根序及土层对细根保存率的影响。结果表明, 伴随时间延长, 细根的保存率逐渐下降, 兴安落叶松细根保存率的下降显著快于水曲柳(p<0.001), 两树种分解期中位值分别为(82±7) d 和(317±28) d; 不同直径等级(≤0.3、0.3～0.6、＞0.6 mm)细根的分解速率不同, 两树种最长分解期中位值均出现在最细直径(≤0.3 mm)根中; 高级根分解速率显著低于一级根(p<0.05); 土壤上层分解速度快, 随着土壤深度增加细根分解速率减小。微根管技术为了解细根自然分解过程提供了有效途径。     

国外对树木细根的研究动态

森林生态系统的研究已经深入到了生态系统的各个层次,但无论是在哪一层次上的研究,其重点往往是树木的地上部分,而对地下部分——根系的研究相对较为薄弱。主要原因是对根系的生态学作用认识不足以及根系研究的困难。近来,随着对根系特别是细根在养分循环及能流中的重要作用的认识,细根的研究已成为森林生态系统研究的一个热点。根系中粗根(直径>5mm)虽然占总生物量的20%左     

中国温带和亚热带8个树种叶和吸收根协同分解

叶和细根(2mm)是森林生态系统的分解主体,二者是否协同分解,将极大影响所属植物在生态系统碳(C)循环中的物种效应。已有研究显示,叶和细根的分解关系具有极大的不确定性,认为很大程度上归因于细根内部具有高度的异质性,导致叶和细根在功能上不相似。为此,使用末梢1级根和细根根枝作为研究对象,它们在功能上同叶类似,称为吸收根。通过分解包法,分别在黑龙江帽儿山和广东鹤山,研究了2个阔叶树种和2个针叶树种(共8个树种)的叶和吸收根持续2a多的分解。结果发现,分解速率k(a~(-1),负指数模型)在8个树种整体分析时具有正相关关系(P0.05),在相同气候带或植物生活型水平上是否相关,受叶的分解环境及吸收根类型的影响;N剩余量整体上并不相关,亚热带树种的叶和细根根枝的N剩余量在分解1a后高度显著正相关,温带树种的叶和1级根的N剩余量在分解2a后显著高度正相关。本研究中,根-叶分解过程是否受控于相同或相关的凋落物性质是决定根-叶分解是否相关的重要原因,其中分解速率与酸溶组分正相关、与酸不溶组分负相关。比较已有研究,总结发现,根-叶分解关系受物种影响较大,暗示气候变化导致物种组成的改变将极大影响地上-地下关系,也因此影响生态系统C循环。     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.