Na2CO3胁迫下星星草幼苗叶绿体GST活性变化及其与相关指标的关系

通过对不同浓度Na2CO3胁迫下星星草幼苗培养基质和叶片渗透势、叶片相对电导率、叶绿体谷胱甘肽转移酶（GST）活性和O2^-产生速率的研究,以探讨星星草幼苗叶绿体GST活性在Na2CO3胁迫下的变化规律及其在抗Na2CO3胁迫中的作用。结果表明,在0～0．4％Na2CO3胁迫范围内,随着其浓度的增加星星草幼苗叶绿体GST活性增强,Na2CO3胁迫浓度继续增加则GST活性急剧减弱。星星草幼苗叶绿体GST活性随培养基质渗透势、叶片渗透势和叶片相对电导率以及叶绿体O2产生速率的变化趋势相似。叶绿体GST活性和Na2CO3胁迫浓度以及叶片渗透势之间、叶绿体GST活性和O2^-产生速率以及叶片渗透势之间、叶绿体GST活性和培养基质渗透势以及叶片渗透势之间、叶绿体GST活性和O2^-产生速率以及叶片相对电导率之间相关关系显著。说明叶绿体GST在星星草幼苗抵抗低强度（浓度）Na2CO3胁迫中起着非常重要的作用。     

PEG模拟干旱胁迫对糜子幼苗生理特性的影响

以'榆糜1号'和'榆糜3号'为试验材料,采用PEG模拟水分胁迫方法,研究了干旱胁迫对糜子幼苗生理生化特性的影响.结果显示,(1)2品种幼苗叶片的细胞电解质外渗率、叶片的MDA含量、游离脯氨酸含量和可溶性糖含量均在胁迫2 d后逐渐上升,但保护酶SOD和POD的活性均呈先升高后降低的变化趋势,2品种幼苗在不同强度PEG胁迫下总体变化趋势基本一致,且各胁迫处理间差异显著(P<0.05).(2)2品种在相同处理下差异显著(P<0.05),其中,10%～30 0A PEG胁迫8 d时,'榆糜3号'比'榆糜1号'的细胞电解质外渗率、叶片的MDA含量增加幅度小,而游离脯氨酸含量和可溶性糖含量增加幅度较大,但保护酶SOD和POD的活性下降幅度较小,说明相同渗透胁迫下'榆糜1号'比'榆糜3号'叶片的细胞膜透性增加幅度大,但渗透调节物质增加较少,细胞膜系统受干旱伤害会更大,其抗旱性相对较弱.综合各项生理指标的分析认为,'榆糜3号'具有较强的抗旱能力.     

松嫩平原两个生态型羊草实验种群对盐碱胁迫的生理响应

采用盆栽实验,对灰绿型和黄绿型两个生态型羊草(Leymus chinensis)在幼苗期分别用不同强度的NaCl、Na2CO3和混合盐碱胁迫,测定其叶片叶绿素含量、电解质外渗率和植株脯氨酸、Na／K等生理指标。结果表明,在3种盐碱胁迫条件下,灰绿型和黄绿型羊草的叶片叶绿素含量、电解质外渗率和植株脯氨酸、Na／K均与胁强之间呈直线y=a+bx变化,达到了显著或极显著水平,两个实验种群均具有耐盐碱能力,叶片叶绿素含量、电解质外渗率和植株脯氨酸、Na／K均有显著或极显著差异,它们在耐盐碱生理特性上已产生了分化,其中,灰绿型的耐盐碱能力强于黄绿型,本文为羊草生态型分化主导生态因子是土壤盐碱所致提供了的生理学证据。     

Cd~(2+)胁迫对小麦幼苗生理生化特性的影响

以小麦品种'西旱2号'和'宁春4号'幼苗为材料,采用室内水培实验研究了不同浓度Cd(NO3)2处理对叶绿素含量、抗氧化酶活性及渗透性调节物含量等的影响.结果表明,两小麦品种幼苗的叶绿素a(Chl a)、叶绿素b(Chl b)及叶绿素总量在镉胁迫下均比对照降低,且高浓度镉对'西旱2号'幼苗叶片Chl b的破坏程度强于Chl a;两品种镉胁迫幼苗的过氧化氢酶(CAT)、过氧化物酶(POD)和抗坏血酸过氧化物酶(APX)活性均比对照不同程度地升高;两品种镉胁迫幼苗的可溶性糖含量均与对照无显著差异,但'宁春4号'幼苗叶片的脯氨酸含量却比对照显著升高,且此效应具有浓度依赖性;镉胁迫下两品种小麦幼苗叶片的MDA含量变化与对照无显著差异.研究显示,两品种小麦幼苗叶片的光合色素在镉胁迫下均受到不同程度的破坏,但它们均能通过增加体内保护酶活性和渗透调节物质含量来缓解膜脂过氧化伤害,从而对镉胁迫均表现出较强的耐受能力.     

盐分和水分胁迫对芦荟幼苗渗透调节和渗调物质积累的影响

用不同浓度NaCl和等渗聚乙二醇(PEG 6000)处理芦荟(Aloe vera L.)幼苗,10 d后测定叶片相对生长速率和厚度、叶片中主要有机溶质、无机离子含量及渗透调节能力.结果表明,-0.44、-0.88 MPa NaCl和PEG处理使芦荟叶片的相对生长速率和叶片厚度明显下降,且盐胁迫对幼苗生长的抑制和叶片含水量降低的效应明显高于等渗的水分胁迫,其叶片渗透调节能力随处理渗透势的降低而增加, -0.88 MPa PEG胁迫的芦荟幼苗的渗透调节能力高于等渗盐分胁迫.在主要渗透调节物质可溶性糖、有机酸、K 、Ca2 和Cl-中,-0.88 MPa PEG处理下含量比相同渗透势的NaCl处理下显著增加的是有机溶质,因此推断有机溶质含量高是PEG胁迫下渗透调节能力较强的主要因素.     

亚精胺浸种对番茄幼苗抗盐碱的生理特性研究

以番茄耐盐碱品种‘金鹏一号’和盐碱敏感品种‘中杂9号’为试验材料,采用营养液水培的方法,设置正常营养液栽培(对照CK)、100mmol/L盐碱溶液胁迫、100mmol/L盐碱溶液胁迫+0.1mmol/L亚精胺(Spd)浸种、100mmol/L盐碱溶液胁迫+0.25mmol/L Spd浸种4种处理,研究外源Spd对番茄幼苗株高和茎粗的相对生长率、叶片和根系含水量、超氧化物歧化酶(SOD)和过氧化物酶(POD)活性以及丙二醛(MDA)、脯氨酸(Pro)、叶绿素含量的影响。结果显示:(1)单独盐碱胁迫下,两品种番茄幼苗叶绿素含量、株高和茎粗的相对生长率、叶片和根系相对含水量较对照均降低,而其MDA、Pro含量、SOD和POD活性显著增加。(2)外源Spd浸种处理较盐碱胁迫下能够增加番茄幼苗的株高和茎粗的相对生长率、叶片和根系的相对含水量、Pro及叶绿素含量,进一步提高SOD和POD的活性,降低其MDA含量,能有效缓解盐碱胁迫对番茄幼苗的伤害。(3)在100mmol/L盐碱胁迫条件下,0.25mmol/L Spd浸种处理对番茄幼苗受到的盐碱胁迫伤害的缓解效果更佳,并且这种缓解作用对盐碱敏感品种‘中杂9号’幼苗的效果更加明显。研究表明,在盐碱胁迫下,番茄幼苗的生长受到一定程度的抑制,但外源Spd浸种能够通过调节渗透调节物质含量、增强抗氧化酶活性来减轻盐碱胁迫的伤害,维持植物体的正常生理代谢功能,从而提高番茄幼苗抵抗盐碱胁迫能力,有效缓解盐碱胁迫的伤害,并以0.25mmol/L Spd浸种处理缓解效果更佳,且这种缓解作用对盐碱敏感品种‘中杂9号’幼苗效果更明显。     

外源调环酸钙对盐碱胁迫下大豆幼苗生长及生理特性的影响

为明确外源调环酸钙(Pro-Ca)缓解大豆幼苗盐碱胁迫的机理,以大豆‘合丰50’为试验材料,研究在110 mmol·L^-1复合盐碱胁迫下,叶面喷施100 mg·L^-1 Pro-Ca对大豆幼苗生长、光合特性、抗氧化代谢、AsA-GSH循环以及渗透调节的影响。结果表明：盐碱胁迫显著抑制大豆幼苗生长,降低了净光合速率(P_n)、叶绿素、可溶性蛋白、可溶性糖、蔗糖和淀粉含量;增加了过氧化氢酶(CAT)活性以及脯氨酸、活性氧(ROS)、丙二醛(MDA)和电解质渗漏率积累;与盐碱处理相比,喷施Pro-Ca能够改善大豆幼苗地上部和根系生长,提高叶绿素a、叶绿素b、类胡萝卜素和总叶绿素含量,维持较高的P_n,促进蔗糖、果糖和淀粉的积累;显著上调叶片6种抗氧化酶(SOD、POD、CAT、GR、MDHAR和DHAR)活性、2种非酶抗氧化剂(AsA和GSH)水平和脯氨酸含量;而电解质渗漏率、O₂^-·产生速率以及MDA和H₂O₂含量显著降低...     

外源硝酸钙对黄瓜幼苗盐胁迫伤害的缓解作用

采用营养液水培法,以较耐盐黄瓜品种'新泰密刺'为试材,研究了叶面喷施硝酸钙对盐胁迫(NaCl 65 mmol·L-1)下黄瓜幼苗生长、叶绿素含量、膜脂过氧化产物丙二醛(MDA)、脯氨酸及不同部位离子含量的影响.结果表明,叶面喷施硝酸钙能够显著提高盐胁迫下黄瓜幼苗的干鲜重、相对含水量和叶片叶绿素含量,显著减少MDA及渗透调节物质脯氨酸的积累;同时可显著降低盐胁迫下黄瓜幼苗体内Na+和Cl-含量,提高K+、Ca2+含量和 K+/Na+、Ca2+/Na+.可见,外源硝酸钙能缓解盐胁迫下黄瓜幼苗的失水程度和光合色素的下降幅度,保护膜的完整性,调节离子选择性吸收,从而减轻盐胁迫伤害,促进黄瓜植株生长.     

外源水杨酸预处理对低温胁迫下甜瓜幼苗生长及其抗逆生理特性的影响

以甜瓜品种‘红优’幼苗为试验材料,在人工气候箱内采用基质栽培法,对其叶面喷施不同浓度(0.1、0.5、1.0、2.0 mmol·L^-1)水杨酸(SA),研究SA预处理对低温(昼12 ℃/夜6 ℃)胁迫7 d及恢复7 d后甜瓜幼苗生长、叶绿素含量、渗透调节物质含量以及抗氧化系统的影响。结果表明：(1)低温胁迫能明显抑制甜瓜幼苗的生长,外源施用不同浓度SA预处理均能缓解低温对甜瓜幼苗的伤害,并以1.0 mmol·L^-1 SA作用最明显,且显著提高了低温胁迫下甜瓜幼苗的株高、茎粗、地上鲜重和叶绿素含量。(2)适宜浓度的外源SA预处理可明显提高低温胁迫下甜瓜幼苗叶片的渗透调节物质可溶性糖、可溶性蛋白和脯氨酸的含量,增强其渗透调节作用。(3)低温胁迫下外源SA预处理能够诱导提高甜瓜幼苗叶片中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)、抗坏血酸过氧化酶(APX)、谷胱甘肽还原酶(GR)和脱氢抗坏血酸还原酶(DHAR)的活性,增加甜瓜幼苗叶片中抗坏血酸(ASA)、谷胱甘肽(GSH)含量、ASA/DHA及GSH/GSSG,从而有效降低叶片电解质渗透率、丙二醛(MDA)和活性氧(ROS)含量。研究发现,适宜浓度的外源SA预处理,能够在低温胁迫条件下通过增加渗透调节物质的含量,诱导增强抗氧化酶活性,以及激活ASA GSH循环系统,促进甜瓜幼苗的生长,从而提高甜瓜幼苗的耐低温性能。     

外源一氧化碳对干旱胁迫下水稻幼苗抗氧化系统的影响

以水稻(Oryza sativa L.) 品种‘D奇宝优1号'幼苗为材料,采用20%聚乙二醇(PEG-6000)模拟水分胁迫,研究外源一氧化碳(CO)对干旱胁迫下水稻幼苗抗氧化能力的影响,以探索CO提高水稻幼苗抗旱性的机制.结果显示,CO供体高铁血红素(Hematin,H)显著降低干旱胁迫下水稻幼苗叶片质膜相对透性和丙二醛(MDA)含量,提高脯氨酸和可溶性蛋白的含量,不同程度地促进叶片中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)的活性,而CO清除剂血红蛋白(Hemoglobin,Hb)则逆转CO供体对干旱胁迫下水稻幼苗氧化损伤的缓解效应.由此表明,外源CO能通过调整保护酶活性和渗透调节物质含量来提高水稻幼苗的抗氧化能力,有效增强其抗旱性.     

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.     

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.     

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.     

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.