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1.
土壤施硒对烤烟生理指标的影响   总被引:7,自引:0,他引:7  
许自成  邵惠芳  孙曙光  郑聪  汪键  闫铁军 《生态学报》2011,31(23):7179-7187
以烤烟品种K326盆栽试验为基础,研究了不同浓度Se对烤烟生长过程中生理特性、烤烟叶片硒含量及硒积累速率的影响.结果表明:低浓度Se(≤8 mg/kg)对烤烟叶片中叶绿素a、叶绿素b、叶绿素a+b和类胡萝卜素含量有促进作用,可提高烤烟叶片中SOD、POD活性;高浓度硒(≥12mg/kg)降低了烤烟叶片SOD、POD活性,烟株生长受到抑制甚至死亡.在适宜的硒浓度范围内,烤烟MDA含量有所降低,缓解了膜脂的过氧化程度;POD活性随着生育期的延长而提高;烤烟生长前期的SOD活性高于后期;烤烟生长中期的MDA含量明显低于前期和后期.随着土壤中硒含量的增加,烤烟叶片中的硒含量逐渐递增,而硒在烤烟叶片中的积累速率呈现出先增高后降低的趋势.  相似文献   

2.
硒蛋白P的研究进展   总被引:1,自引:0,他引:1  
硒蛋白P(SeP)是从大鼠和人血浆中分离、纯化得到的一种糖蛋白 ,每个硒蛋白P多肽含有10个硒代半胱氨酸。硒蛋白P中的硒含量占大鼠和人血浆中硒含量的 5 0 %以上。在其mRNA开放阅读框架中克隆的cDNA的序列含有 10个UGA密码子。硒代半胱氨酸在一个UGA密码子处嵌入蛋白的一级结构 ,尽管对硒蛋白P功能还没有彻底了解 ,它的一种非常可能的作用是作为一种胞外抗氧化剂。大鼠血浆中的硒蛋白P在体内实验中对Diquat诱导的脂质过氧化和肝损坏具有保护作用 ,人血浆中的硒蛋白P在体外实验中显示减少内毒素过氧化硝酸盐和磷脂氢过氧化物的活性。牛血浆中的硒蛋白P在神经细胞的培养中作为一存活促进因子。  相似文献   

3.
镉诱发肝细胞毒性和胞内Ca2+变化及硒的保护作用研究   总被引:5,自引:0,他引:5  
本文通过研究镉诱发鼠肝细胞毒性和胞内游离Ca2 变化及硒的干预效应,探讨镉致肝细胞损伤机制及硒的保护作用。分离培养新生鼠原代肝细胞,随机分为正常对照组、4个5、25、100和250μmol/LCdCl2组、2个10和20μmol/LNa2SeO3组和8个用10和20μmol/LNa2SeO3分别与5、25、100和250μmol/LCdCl2联合作用组。在实验后第12h检测肝细胞存活及其MDA含量和培养液中LDH活性,激光共聚焦显微镜分析肝细胞内游离Ca2 水平([Ca2 ]i)。结果显示,镉处理的肝细胞存活随镉浓度增加明显下降,硒处理组与对照组差异不明显;硒提高或明显提高镉染毒肝细胞存活。肝细胞培养上清液LDH活性随镉浓度增加而逐渐升高,且100和250μmol/LCdCl2组显著高于对照组,而硒处理组未见明显变化;给予硒的25、100和250μmol/LCdCl2处理组LDH活性下降或明显下降。不同浓度镉均诱发肝细胞MDA含量显著升高,而硒处理组未见类似表现;10和20μmol/LNa2SeO3抑制或显著地降低25、100和250μmol/LCdCl2诱发的MDA的生成。经镉处理的肝细胞[Ca2 ]i荧光强度明显高于对照组,且随镉浓度的增加而上升,而给予硒的肝细胞[Ca2 ]i荧光强度未见升高,与对照组相近;加入硒的镉染毒肝细胞[Ca2 ]i均比各对应浓度的镉处理组有较大幅度地下降,其中给予硒的25μmol/LCdCl2处理组差异显著,且接近对照组的水平。结果提示,镉诱发肝细胞毒性和损伤以及肝细胞[Ca2 ]i升高;硒可能通过干预肝损伤细胞脂质过氧化反应,改善和保护肝细胞[Ca2 ]i稳态而减轻镉诱发的细胞毒性和损伤过程。  相似文献   

4.
饲料硒和维生素E对大鼠机体抗氧化能力的影响   总被引:1,自引:0,他引:1  
 用克山病病区粮配成基础低硒饲料,补充硒和/或维生素E组成四种不同水平的饲料,饲喂雄性断乳大鼠,观察其对机体抗氧化能力的影响。评价指标是用抗坏血酸诱发的红细胞溶血率、被O~-_2(超氧阴离子)氧化的血红蛋白量和组织中的TBA值。动物饲养13周后,自尾静脉取血,测定溶血率和血红蛋白被氧化的百分率,和全血SeGSHPx(含硒谷胱甘肽过氧化物酶)活力。15周后将动物断头杀死,立即取出心脏和肝脏测定SeGSHPx活力和TBA值。结果表明在克山病病区粮的饲料中补充硒或维生素E,或者二者同时补充均明显提高组织中的SeGSHPx活力和降低组织中的TBA值。不论在硒缺乏时或硒充足时,饲料中补充维生素E显著降低抗坏血酸诱发的红细胞溶血率,对O~-_2氧化血红蛋白无保护作用。在维生素E缺乏时,仅补充硒对溶血无作用。不论饲料中维生素E缺乏或者充足,补充硒对O~-_1氧化血红蛋白均有显著保护作用。  相似文献   

5.
硒的抗自由基损伤作用   总被引:2,自引:0,他引:2  
用黄嘌呤-黄嘌呤氧化酶体系或低硒饲料诱发自由基损伤。在培养的鼠心肌细胞上,硒能使受损心肌细胞的自由基含量、超微结构、动作电位、膜输入阻抗恢复正常;在离体灌流的鼠心上,硒能改善受损心脏的心肌收缩性能;硒能使受损鼠的心硒含量与肝谷胱甘肽过氧化物酶(GSH_(ps))活力回升、肝过氧化脂质(LPO)含量下降。上述结果提示硒保护作用的基本机制可能与增强GSH_(px)活力、促进自由基清除有关。  相似文献   

6.
本文观察了低硒的克山病病区粮和克山病病区粮补硒后喂养大鼠对其红细胞膜脂流动性的影响。实验结果表明克山病病区粮喂养的大鼠红细胞膜脂流动性较正常对照降低,其原因可能与机体处于低硒状态下红细胞膜结合硒含量降低、红细胞膜胆固醇含量及脂质过氧化产物升高有关,克山病病区粮补硒后喂养大鼠,其红细胞膜脂流动性恢复至正常对照。  相似文献   

7.
摘要 目的:检测硒(NaSe)对CoCl2氧化应激诱导人胎盘滋养层细胞(JEG-3) 增殖与凋亡的影响及其可能机制。方法:体外培养JEG-3 细胞,在加入CoCl2(500 μM)氧化应激诱导前先加入NaSe(100nM) 预处理24小时,MTT 实验检测硒对氧化应激JEG-3的增殖促进作用; 利用细胞流式术(FCM)检测硒对氧化应激JEG-3细胞凋亡的影响;用Western blot检测硒影响氧化应激JEG-3细胞增殖与凋亡的可能分子生物学机制。结果:MTT 提示硒能够增加氧化应激诱导的JEG-3细胞的增殖活性(P<0.05) ,降低氧化应激JEG-3细胞凋亡率(P<0.01) ,同时硒蛋白Gpx1表达上调(P<0.05) ,脂质过氧化物MDA表达下降(P<0.05)。结论:硒通过上调硒蛋白Gpx1 表达,降低脂质过氧化物MDA表达,进而降低氧化应激JEG-3细胞凋亡率而发挥其促进增殖活性,提示硒的补充对子痫前期的预防和治疗具有重要的意义。  相似文献   

8.
硒蛋白P的研究进展   总被引:4,自引:0,他引:4  
硒蛋白P(SeP)是从大鼠和人血浆中分离,纯化得到的一种糖蛋白,每个硒蛋白P多肽含有10个硒代半胱氨酸,硒蛋白P中的硒含量占大鼠和人血浆中硒含量的50%以上,在其mRNA开放阅读框架中克隆的cDNA的序列含有10个UGA密码子。硒代半胱氨酸在一个UGA密码子处嵌入蛋白的一级结构,尽管对硒蛋白P功能还没有彻底了解,它的一种非常可能的作用是作为一种胞外抗氧化剂,大鼠血浆中的硒蛋白P在体内实验中对Diquat诱导的脂质过氧化和肝损坏具有保护作用,人血浆中的硒蛋白P在体外实验中显示减少内作为一存活促进因子。  相似文献   

9.
硒对镉胁迫下水稻幼苗生长及生理特性的影响   总被引:51,自引:0,他引:51  
采用溶液培养 ,研究不同浓度的硒和镉处理对稻苗的株高、叶片干重、叶绿素、还原糖、叶片丙二醛含量以及保护酶 SOD、POD、CAT活性的影响。结果表明 ,镉胁迫下稻苗矮化 ,镉毒害使叶片失绿 ,干重降低 ,还原糖含量下降 ,叶片 MDA含量增加 ,POD活性增强 ,而 SOD、CAT活性降低 ;硒可减轻镉对水稻的毒害 ,表现为 :减轻镉胁迫对株高增加的抑制 ,提高叶绿素含量 ,增加叶片干物质积累 ,提高叶片还原糖含量 (Cd0 .5 mg/ L加 Se 0 .1 0~ 0 .5 0 mg/ L例外 ) ,降低 MDA含量与 POD活性 ,提高 SOD、CAT活性  相似文献   

10.
本实验选用SD(Sprague Dawley)大鼠,建立大强度耐力训练模型,研究迷迭香对运动大鼠肝脏组织脂质过氧化损伤保护作用。结果显示,1)迷迭香可降低血清丙氨酸氨基转移酶活性,升高肝组织丙氨酸氨基转移酶的活性,都有显著性差异(P<0.05);2)迷迭香可以不同程度地增强肝脏组织中抗氧化酶SOD(superoxide dis-mutase)、CAT(catalase)和GSH-Px(glutathione peroxidase)的活性,其中SOD和CAT的活性增加在安静和运动状态下都有显著性差异(P<0.05),GSH-Px的活性增加在运动状态下具有显著性差异(P<0.05);3)迷迭香可以降低肝脏组织中MDA(malondialdehyde)的含量,无显著性差异(P>0.05)。结论:迷迭香可以增加肝脏组织中的抗氧化酶活性,减轻大强度耐力训练对大鼠肝脏组织造成的脂质过氧化损伤。并且在同一状态下对不同的抗氧化酶活性影响不同。  相似文献   

11.
目的:研究肺叶切除术对红细胞及淋巴细胞膜流坳性的影响。方法:选择20例择期开胸手术病人,均作肺叶切除术。分别用微量滴定法、高效液权色谱法和DPH荧光探剂法测定血浆和红细胞膜PLA2活性,红细胞膜磷脂PS、PE、PC和红细胞、淋巴膜脂流动性。结果:手术10min、手术60min和手术结束后30min血浆和红细胞膜PLA2活性均显著高于麻醉诱导前;手术60min和手术结束后30min 红细胞膜PS、P  相似文献   

12.
为探究饲料中高剂量的有机硒和无机硒对异育银鲫(Carassius auratus gibelio var. CAS V)的生长性能、硒蓄积和血浆生化指标等方面的影响,以硒代蛋氨酸(有机硒)和亚硒酸钠(无机硒)作为不同类型的硒源,初始体重为(62.95±0.23) g异育银鲫为研究对象,进行了为期90d的养殖实验。实验结果表明,饲料中添加0、10和20 mg/kg的有机硒和无机硒对异育银鲫的存活和饲料干物质的表观消化率无显著影响;有机硒处理组硒的表观消化率随饲料有机硒的添加量增加而显著升高(P<0.05);饲料中添加无机硒对硒消化率无显影响(P>0.05)。在饲料中添加有机硒可以提高异育银鲫的生长(P<0.05),在20 mg/kg处理组中达到最高(P<0.05);而饲料中添加10 mg/kg无机硒处理组未显著改变异育银鲫的特定生长率(P>0.05),但高浓度的无机硒则显著降低了其特定生长率(P<0.05)。饲料中添加有机硒显著降低了异育银鲫的肝体比,添加10 mg/kg无机硒显著降低异育银鲫的肝体比(P<0.05);饲料中添加有机硒和无机硒对异...  相似文献   

13.
 研究了温室种植的小麦在0kJ·m-2(对照)、8.82kJ·m-2(处理1)和12.6kJ·m-2(处理2)3种剂量的紫外线B辐射下叶绿体膜组分和膜流动性的变化。紫外线B辐射导致了光合色素(包括叶绿素和类胡萝卜素)的降解、Hill反应的抑制、膜脂肪酸组分配比的改变和不饱和度指数(IUFA)的下降、膜流动性的降低以及丙二醛(MDA)含量的升高。分析表明,紫外线B辐射诱导的膜脂过氧化是叶绿体膜系统受破坏的主要原因。  相似文献   

14.
The effect of Ep on different ATPases and acetylcholinesterase of rat RBC membrane was studied. Starvation caused a slight decrease in Mg2+-, Ca2+-, and Na+ + K+-ATPases. However, these enzyme activities were markedly increased on Ep treatment of starved rats. Specific activities of all three ATPases increased linearly with increasing concentration of Ep. Under identical conditions the hormone failed to stimulate the ATPase activity of liver plasma membrane. Desensitization by fluoride of allosteric inhibition of erythrocyte membrane-bound Na+ + K+-ATPase was observed under starvation which showed a return to normal n values on Ep administration. The enzyme from normal animals was inhibited almost completely at 0.1 mM fluoride whereas enzyme from starved and Ep-treated animals showed only about 50% inhibition at that fluoride concentration. Ep increased the acetylcholinesterase activity of normal RBC membrane to a small extent whereas the stimulation was much higher under starvation. The fluoride inhibition curve of this enzyme changed from sigmoidal to hyperbolic under starvation which again changed to allosteric on administration of Ep. These changes were closely correlated to n values. Red blood cells of Ep-treated animals became more susceptible to osmotic shock under the experimental conditions.  相似文献   

15.
Significant amounts of di(2-ethylhexyl) phthalate (DEHP) leach out into blood stored in DEHP plasticized polyvinyl chloride (PVC) bags resulting in the exposure of recipients of blood transfusion to this compound. The aim of this study was to find out whether DEHP at these low levels has any effect on the activity of membrane Na(+)-K+ ATPase, since a decrease in this enzyme activity has been reported to take place in a number of disorders like neurodegenerative and psychiatric disorders, coronary artery disease and stroke, syndrome-X, tumours etc. DEHP was administered (ip) at a low dose of 750 microg/100 g body weight to rats and the activity of membrane Na(+)-K+ ATPase in liver, brain and RBC was estimated. Histopathology of brain, activity of HMG CoA reductase (a major rate limiting enzyme in the isoprenoid pathway of which digoxin, the physiological inhibitor of Na(+)-K+ ATPase is a product), intracellular concentration of Ca2+ and Mg2+ in RBC (which is altered as a result of inhibition of Na(+)-K+ ATPase) were also studied. (In the light of the observation of increase of intracellular Ca2+ load and intracellular depletion of Mg2+ when Na(+)-K+ ATPase is inhibited). Histopathology of brain revealed areas of degeneration in the rats administered DEHP. There was significant inhibition of membrane Na(+)-K+ ATPase in brain, liver and RBC. Intracellular Ca2+ increased in the RBC while intracellular Mg2+ decreased. However activity of hepatic HMG CoA reductase decreased. Activity of Na(+)-K+ ATPase and HMG CoA reductase, however returned to normal levels within 7 days of stopping administration of DEHP. The inhibition of membrane Na(+)-K+ ATPase activity by DEHP may indicate the possibility of predisposing recipients of transfusion of blood or hemodialysis to the various disorders mentioned above. However since this effect is reversed when DEHP administration is stopped, it may not be a serious problem in the case of a few transfusion; but in patients receiving repeated blood transfusion as in thalassemia patients or patients undergoing hemodialysis, possibility of this risk has to be considered. This inhibition is a direct effect of DEHP or its metabolites, since activity of HMG CoA reductase, (an enzyme which catalyses a major rate limiting step in the isoprenoid pathway by which digoxin, the physiological inhibitor of Na(+)-K+ ATPase is synthesized) showed a decrease.  相似文献   

16.
Data reviewed here indicate that acute and chronic ethanol ingestion induce a decrease in the concentration of GSH and an increase in lipoperoxidation in the liver both in experimental animals and in man, changes that are closely interrelated GSH depletion is suggested to be due to an oxidation in the liver tissue and to a translocation into the extrahepatic medium as free glutathione and/or as conjugates with ethanol-derived acetaldehyde. As a result, the hepatic GSH/GSSG ratio is drastically reduced. Lipoperoxidation seems to be related to the metabolism of ethanol and acetaldehyde by secondary pathways that are known to generate oxygen-related free radicals. Being lipoperoxidation a process associated with cell damage and death, its stimulation by ethanol ingestion could play a role in the production of alcoholic liver damage in man. The involvement of several contributory factors in the development of a high lipoperoxidative index in the liver in this situation is discussed.  相似文献   

17.
It has been proposed that interaction of catecholamines and indoleamines with free radicals may result in the formation of endogenous neurotoxins. In order to better understand the mechanisms involved in neurodegenerative disorders showing evidence of oxidative stress, we have studied the basal concentrations and the turnover rates of dopamine, noradrenaline, serotonin and their metabolites in the prefrontal cortex of rats that were fed on control or low selenium diets. Nutritional deficit of selenium decreases the brain antioxidant protection in experimental conditions by the decrease in glutathione peroxidase activity.

The dopamine and serotonin turnover increased and noradrenaline and 5-hydroxy-3-indoleacetic acid turnover decreased compared to experimental control animals. The increase of dopamine turnover in experimental rats was accompanied by an increase in tyrosine hydroxylase activity. These results suggest that the decrease of brain protection against oxidative damage could induce brain damage by disturbing the turnover rate of some monoamines.  相似文献   


18.
 本文为探讨硒抗肿瘤的机理而开展了硒对小鼠腹水型肝癌(Hep.A)细胞膜流动性影响的研究。结果表明;1.腹水型肝癌细胞膜流动性明显高于正常肝细胞的膜流动性。2.硒能显著降低腹水型肝癌细胞膜的流动性,而对正常肝细胞的膜流动性没有明显影响。3.通过降低腹水型肝癌细胞膜的流动性,可降低肿瘤细胞的致癌力。  相似文献   

19.
Although the effects of red blood cell (RBC) aggregation on low-shear rate blood viscosity are well known, the effects on in vivo flow resistance are still not fully resolved. The present study was designed to explore the in vivo effects of RBC aggregation on flow resistance using a novel technique to enhance aggregation: cells are covalently coated with a block copolymer (Pluronic F-98) and then suspended in unaltered plasma. RBC aggregation was increased in graded steps by varying the Pluronic concentration during cell coating and was verified by microscopy and erythrocyte sedimentation rate (ESR), which increased by 200% at the highest Pluronic level. RBC suspensions were perfused through an isolated in situ guinea pig hindlimb preparation while the arterial perfusion pressure was held constant at 100 mmHg via a pressure servo-controlled pump. No significant effects of enhanced RBC aggregation were observed when studies were conducted in preparations with intact vascular control mechanisms. However, after inhibition of smooth muscle tone (using 10(-4) M papaverin), a significant change in flow resistance was observed in a RBC suspension with a 97% increase of ESR. Additional enhancements of RBC aggregation (i.e., 136 and 162% increases of ESR) decreased flow resistance almost to control values. This was followed by another significant increase in flow resistance during perfusion with RBC suspensions with a 200% increase of ESR. This triphasic effect of graded increases of RBC aggregation is most likely explained by an interplay of several hemodynamic mechanisms that are triggered by enhanced RBC aggregation.  相似文献   

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