一氧化氮介导细胞凋亡的分子基础

一氧化氮作为细胞内生物信使或细胞毒性分子介导细胞凋亡。阐述一氧化氮启动细胞凋亡与抑制细胞凋亡的复杂分子机制。     

丛枝菌根真菌诱导植物信号物质研究进展

丛枝菌根(AM)真菌侵染植物根系形成菌根共生体过程中能诱导植物合成多种信号物质,如水杨酸(SA)、茉莉酸(JA)、类黄酮、一氧化氮(NO)和过氧化氢(H2O2)等。这些信号分子的传导途径和作用机制备受关注。本文从AM真菌诱导植物信号物质的种类和数量入手,探讨这些信号分子在植物体内的传导途径、生理效应和可能的作用机制,旨在为研究AM真菌与植物之间的共生关系、功能与进化等提供依据。     

浮游植物中一氧化氮的生理作用研究进展

一氧化氮（NO）作为一种具有生物活性的气体自由基分子,它的功能代表了生物学系统中信号传递的新途径。大量证据表明,NO在浮游植物细胞中的功能和在高等动植物中类似,具有调节生长和参与抗逆性的作用,NO和ROS可能作为信号分子参与介导浮游植物程序性死亡（PCD）过程。文章较全面地介绍了NO在浮游植物中的产生途径、测定方法、生理功能和PCD的关系及作为信号分子的作用,并对该领域今后的研究进行了展望。     

一氧化氮诱导细胞调亡

一氧化氮(NO)参与体内众多的生理病理过程,最近发现NO与细胞凋亡关系密切,可诱发多种细胞发生凋亡,并与其他活性氧自由基(ROS)的凋亡传导途径之间存在对话效应,NO诱导凋亡促进p53基因表达,其分子作用机理正是目前的研究重点。     

一氧化氮与雄性生殖系统

一氧化氮是近年来发现的一种重要的生物信号分子和效应分子 ,在生物体内 ,L 精氨酸在一氧化氮合酶的作用下生成一氧化氮后 ,以自分泌或旁分泌形式作用于自身或邻近的细胞 ,发挥信号传导和细胞毒性等多种生理功能。近年来的研究表明 ,一氧化氮对雄性生殖系统上至下丘脑 ,下到性腺、附性器官都具有十分重要的生理调节作用。     

NO通过水杨酸(SA)或者茉莉酸(JA)信号途径介导真菌诱导子对粉葛悬浮细胞中葛根素生物合成的促进作用

一氧化氮(NO)是近年来发现对植物细胞次生代谢产物合成具有调控作用的一种新型信号分子. 为了研究NO对植物细胞次生代谢调控的信号转导机理, 考查了在真菌诱导子作用下粉葛悬浮细胞中NO, 水杨酸(SA), 茉莉酸(JA)及葛根素含量的变化情况. 试验结果表明, 真菌诱导子可以诱发粉葛细胞的NO迸发、SA合成和葛根素含量增加, 但细胞中JA水平未发生明显变化. NO猝灭剂cPITO可以阻断真菌诱导子对粉葛细胞中SA和葛根素合成的促进作用, 说明NO是介导真菌诱导子诱发粉葛细胞中葛根素和SA生物合成所必需的上游信号分子. 在缺乏SA积累能力的NahG转基因粉葛细胞中, 真菌诱导子虽然不能促进SA积累, 但仍然可以诱发NO迸发和葛根素生物合成, 并且促进细胞中JA的合成积累. cPITO可以抑制真菌诱导子对NahG转基因粉葛细胞中JA合成的诱导作用, 说明JA是作用于NO下游的信号分子. JA合成抑制剂IBU和NDGA可以抑制外源NO对NahG转基因粉葛细胞中葛根素生物合成的促进作用, 说明NO依赖JA诱发NahG转基因粉葛细胞中葛根素的生物合成. 外源SA处理可以显著降低真菌诱导子对NahG转基因粉葛细胞中JA合成的促进作用, 并逆转IBU和NDGA对NO和真菌诱导子诱发葛根素合成的抑制作用, 说明SA可以抑制细胞中JA的生物合成; 而且当JA合成受到抑制时, SA可以替代JA介导NO和真菌诱导子对葛根素合成的促进作用. 由于真菌诱导子可以促进野生型粉葛细胞中SA的生物合成, 我们推测在野生型粉葛细胞中, 真菌诱导子可能通过诱发SA合成积累抑制了其对细胞中JA合成的促进作用, NO可能主要通过SA信号途径介导真菌诱导子对细胞中葛根素生物合成的促进作用. 而在SA积累受阻的NahG转基因粉葛细胞中, NO则通过激活JA的生物合成并依赖JA信号途径介导真菌诱导子促进粉葛细胞中葛根素的生物合成.     

酒精诱导突触发生期神经元凋亡的分子机理

在突触发生时期,酒精诱导的神经元凋亡可能是胎儿酒精综合征产生的原因之一。酒精可能通过增加自由基的产生,影响神经递质受体的功能、干扰神经营养因子信号通路、激活内源性的细胞凋亡信号途径等分子机制,促进发育过程中的神经元凋亡。酒精影响发育的另一个重要机制是抑制蛋白质合成。新近的研究显示,双链RNA激活的蛋白激酶介导酒精引起的蛋白翻译受阻和神经元死亡。     

运动对线粒体介导骨骼肌细胞凋亡信号通路的影响

细胞凋亡是一种程序化的细胞死亡方式,其信号传导通路分为外源性和内源性两条主要途径,线粒体在内源性细胞凋亡途径中扮演着重要的角色.研究表明,运动可通过调节线粒体介导骨骼肌细胞凋亡的进程,而运动调节线粒体介导骨骼肌细胞凋亡信号通路影响机体细胞生物进程的机制仍有待研究.该文主要阐述了线粒体介导细胞凋亡信号传导通路及运动对其的...     

一氧化氮诱导细胞凋亡

一氧化氮(NO)参与体内众多的生理病理过程,最近发现NO与细胞凋亡关系密切,可诱发多种细胞发生凋亡,并与其他活性氧自由基(ROS)的凋亡传导途径之间存在对话效应,NO诱导凋亡促进p53基因表达,其分子作用机理正是目前的研究重点.     

整合素及其信号传导通路

整合素是位于细胞表面的重要黏附分子,通过其双向信号传导通路,介导细胞与细胞外基质及细胞与细胞间的黏附.整合素由胞外域、跨膜域和胞内域3部分组成.胞内域与细胞内信号分子结合,启动胞内一胞外信号传导激活整合素,提高与相应配体亲合力.而胞外域与相应配体结合后,通过胞外-胞内信号传导,调节细胞生存、增殖、黏附、分化功能.近年研究显示,整合素结构功能及信号传导通路异常与多种疾病有关.     

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.     

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.     

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.