Ascorbate plays a key role in alleviating low temperature-induced oxidative stress in Arabidopsis

Low temperature has a negative impact on plant cells and results in the generation of reactive oxygen species (ROS). In order to study the role of ascorbate under chilling stress, the response of an ascorbate-deficient Arabidopsis thaliana mutant vtc2-1 to low temperature (2°C) was investigated. After chilling stress, vtc2-1 mutants exhibited oxidative damage. An increase in the H₂O₂ generation and the production of thiobarbituric acid reactive substances (TBARS), and a decrease in chlorophyll content, the maximal photochemical efficiency of PSII (F_v/F_m) and oxidizable P₇₀₀ were also noted. The ratio of ascorbate/dehydroascorbate and reduced glutathione/oxidzed glutathione in the vtc2-1 mutants were reduced, compared with the wild type (WT) plants. The activities of antioxidant enzymes, such as catalase (CAT) and ascorbate peroxidase (APX), and soluble antioxidants were lower in the vtc2-1 mutants than those in WT plants. These results suggested that the ascorbate-deficient mutant vtc2-1 was more sensitive to chilling treatment than WT plants. The low temperature-induced oxidative stress was the major cause of the decrease of PSII and PSI function in the vtc2-1 mutants. Ascorbate plays a critical role of defense without which the rest of the ROS defense network is unable to react effectively.     

高温诱导黄瓜抗霜霉病机理

研究了高温对黄瓜霜霉病菌致病力的影响以及高温控制霜霉病发生的效果.结果表明,40 ℃高温处理2 h和45 ℃处理1 h对黄瓜霜霉病的诱导抗病性作用最明显,其在接种后4 d时的防效分别为58.40%和45.81%,到接种后6 d时,防效分别下降为39.35%和37.65%.经高温诱导后,过氧化物酶（POD）、苯丙氨酸解氨酶(PAL)、几丁质酶（Cht）、β-1,3-葡聚糖酶（Glu）活性均显著高于对照,与未诱导植株相比,高温诱导后叶片组织的细胞壁表面有大量木质素沉积,表明高温处理后黄瓜表现出对霜霉病的抗病性.     

Arbuscular mycorrhizae improve low temperature tolerance in cucumber via alterations in H2O2 accumulation and ATPase activity

The combined effects of arbuscular mycorrhizal fungi (AMF) and low temperature (LT) on cucumber plants were investigated with respect to biomass production, H₂O₂ accumulation, NADPH oxidase, ATPase activity and related gene expression. Mycorrhizal colonization ratio was gradually increased after AMF-inoculation. However, LT significantly decreased mycorrhizal colonization ability and mycorrhizal dependency. Regardless of temperature, the total fresh and dry mass, and root activity of AMF-inoculated plants were significantly higher than that of the non-AMF control. The H₂O₂ accumulation in AMF-inoculated roots was decreased by 42.44 % compared with the control under LT. H₂O₂ predominantly accumulated on the cell walls of apoplast but was hardly detectable in the cytosol or organelles of roots. Again, NADPH oxidase activity involved in H₂O₂ production was significantly reduced by AMF inoculation under LT. AMF-inoculation remarkably increased the activities of P-type H⁺-ATPase, P-Ca²⁺-ATPase, V-type H⁺-ATPase, total ATPase activity, ATP concentration and plasma membrane protein content in the roots under LT. Additionally, ATP concentration and expression of plasma membrane ATPase genes were increased by AMF-inoculation. These results indicate that NADPH oxidase and ATPase might play an important role in AMF-mediated tolerance to chilling stress, thereby maintaining a lower H₂O₂ accumulation in the roots of cucumber.     

The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

As a part of the nitroso signalling pathway, nitroso-compounds serve as stores and carriers of NO; as part of the sulphide signalling pathway, bound sulfane-sulphur compounds serve as stores and carriers of H2S. Here we hypothesise a coupled sulphide-nitroso signalling pathway, in which H2S plays a main role. H2S releases NO from the endogenous S-nitroso-compounds nitroso-cysteine, nitroso-acetylcysteine and nitroso-albumin. Relaxation of noradrenaline-precontracted aortic rings by H2S is also enhanced in the presence of nitroso-albumin, which may implicate the involvement of the nitroso signalling pathway. Pretreatment of albumin, cysteine, N-acetylcysteine and lipids with H2S results in binding of sulphur to these compounds creating thus new-modified sulphur compounds that release NO from nitroso-compounds directly and/or through released H2S, which suggests sulphide-nitroso signalling pathway participation. This hypothesis is supported by the observation that the pretreatment of noradrenaline-precontracted aortic rings with H2S significantly enhanced relaxation induced by nitroso-glutathione in the absence of H2S. We assume that the NO release from nitroso-compounds directly by H2S or indirectly by the H2S-induced sulphur-bound compounds represents coupled sulphide-nitroso signalling, which may explain some of the numerous biological effects of H2S that are shared with NO.     

The role of Na2S in anoxygenic photosynthesis and H2 production in the cyanobacterium Nostoc muscorum

Na2S is known to support anoxygenic photosynthesis in some strains of cyanobacteria and to stimulate H2 production in N2 fixing filaments of Nostoc muscorum. We have shown electron transfer between Na2S and Photosystem I to be dependent on cytochrome b559 which was detected only in vegetative cells. An electron mediator was required to support Na2S driven nitrogenase activity in isolated heterocysts. Na2S was also found to deplete the ATP pool, probably by inhibiting electron transfer from Photosystem I.     

The presenilin 1 C92S mutation increases abeta 42 production

Although wild-type human presenilin 1 (PS1) rescues the C. elegans egg-laying (egl) phenotype that is caused by a loss of function mutation in the C. elegans presenilin homologue sel12, most familial Alzheimer's disease (FAD)-linked PS1 mutants only partially rescue this phenotype. To investigate the effects of the loss of function sel12 mutation on Abeta production in mammalian cells, we analyzed Abeta production in transfected H4 neuroglioma cells expressing the PS1 homologue of the sel12 C60S mutant, PS1 C92S. This analysis revealed that PS1 C92S increased Abeta42 levels in a similar fashion to other pathogenic Alzheimer's disease (AD) PS1 mutations. Significantly, the PS1 C92S mutation has recently been identified as the pathogenic mutation in an Italian family with FAD. Thus, placing a mutation that results in loss of function in C. elegans into a context whereby its effect on mammalian cells can be evaluated suggests that all FAD-linked PS1 mutants result in increased Abeta42 production through a partial loss of function mechanism.     

The role of light in formation of modified S2-state upon low pH-treatment of oxygen-evolving Photosystem II

An abnormal, structurally modified, kinetically stable S₂-state has been reported to be induced when Photosystem II was treated with NaCl-EGTA (or EDTA) in the light or with pH in darkness, both are assumed to release functional Ca²⁺. In order to compare the mechanism of induction of modified S₂-state between the two treatments, effects of illumination during or before low pH-treatment on formation of the abnormal S₂-state were investigated by means of thermoluminescence measurements and low temperature EPR spectroscopy. Following results have been obtained: Flash illumination during low pH-treatment did not practically induce the abnormal S₂-state, whereas preflash illumination given immediately before low pH-treatment efficiently induced the abnormal S₂-state, and its amplitude showed a period-four oscillation on varying the preflash number with maxima at the second and sixth flashes. The abnormal S₂-state thus induced by preflashes was identical with the modified S₂-state that could be induced in dark-low pH-treated Photosystem II by excitation at 0°C after neutralization to pH 6.5. It was inferred that in low pH-treatment, modified S₂-state can be formed from both S₂- and S₃-states, but its yield from the latter is much higher than from the former, consistent with the early results by Boussac et al. obtained for NaCl-EGTA-light or NaCl-citrate-light treatment.Abbreviations DCMU 3-(3,4-dichlorophenyl)-1,1-dimethylurea - EDTA ethylenediaminetetraactate - EGTA ethylene glycol bis(-aminoethylether)-N,N,N,N-tetraacetic acid - Mes 2-(N-morpholino)ethanesulfonic acid - PS II Photosystem II     

95Mo NMR spectra of MoO2(C8H7N2S)2 and X-ray crystal structure of Mo2O4(C8H7N2S)2(C3H7NO)2

The facile preparation of MoO₂(C₈H₇N₂S)₂ is given and its complex behaviour in dimethylformamide, as revealed by ⁹⁵Mo NMR spectroscopy, discussed. The X-ray crystal structure of one of the products obtained from this dimethylformamide solution is briefly described. This structure indicates that the Mo(VI) has been reduced to Mo(V) and is based on the [Mo₂O₄]²⁺ core.     

H2-calponin在细胞力学信号感知中的作用

H2-calponin是一种肌动蛋白细胞骨架结合蛋白,在平滑肌细胞和一些非肌肉细胞中均有表达,并且在发育及重建的组织中高表达。H2-calponin作为一种机械应力的胞内应答因子,受机械应力调节,通过与细胞骨架F-肌动蛋白(F-actin)及多种粘着斑蛋白相互作用,参与细胞力学信号感受与传导,在调节细胞增殖、分化、迁移以及胞质分裂等生理活动中起着重要作用。本文在介绍H2-calponin生化特征的基础上,对其在细胞应力感受及力学信号转导中的作用做一综述。     

Hyperoxia increases H2O2 production by brain in vivo

Hyperoxia and hyperbaric hyperoxia increased the rate of cerebral hydrogen peroxide (H2O2) production in unanesthetized rats in vivo, as measured by the H2O2-mediated inactivation of endogenous catalase activity following injection of 3-amino-1,2,4-triazole. Brain catalase activity in rats breathing air (0.2 ATA O2) decreased to 75, 61, and 40% of controls due to endogenous H2O2 production at 30, 60, and 120 min, respectively, after intraperitoneal injection of 3-amino-1,2,4-triazole. The rate of catalase inactivation increased linearly in rats exposed to 0.6 ATA O2 (3 ATA air), 1.0 ATA O2 (normobaric 100% O2) and 3.0 ATA O2 (3 ATA 100% O2) compared with 0.2 ATA O2 (room air). Catalase inactivation was prevented by pretreatment of rats with ethanol (4 g/kg), a competitive substrate for the reactive catalase-H2O2 intermediate, compound I. This confirmed that catalase inactivation by 3-amino-1,2,4-triazole was due to formation of the catalase-H2O2 intermediate, compound I. The linear rate of catalase inactivation allows estimates of the average steady-state H2O2 concentration within brain peroxisomes to be calculated from the formula: [H2O2] = 6.6 pM + 5.6 ATA-1 X pM X [O2], where [O2] is the concentration of oxygen in ATA that the rats are breathing. Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.     

Mehler reaction plays a role in C3 and C4 photosynthesis under shade and low CO2

Photosynthesis Research - Alternative electron fluxes such as the cyclic electron flux (CEF) around photosystem I (PSI) and Mehler reaction (Me) are essential for efficient photosynthesis because...     

Anaerobic digestion modelling — The role of H2

A dynamic model of a continuous glucose-fed digester is presented, including hydrogen inhibition of acetogenesis and pH inhibition of methanogens. Unionised volatile fatty acids are not considered toxic. Hydrogen concentration could be a useful stability parameter.     

Ionomycin causes susceptibility to phospholipase A2 while temperature-induced increases in membrane fluidity fail: Possible involvement of actin fragmentation

A diminution in the order of membrane lipids, which occurs during apoptosis, has been shown to correlate with increased membrane susceptibility to hydrolysis by secretory phospholipase A₂. Studies with artificial membranes, however, have demonstrated that the relationship between membrane order and hydrolysis is more complex than suggested thus far by cell studies. To better resolve this relationship, this study focused on comparisons between increasing temperature and calcium ionophore as means of decreasing membrane order in S49 cells. Although these two treatments caused comparable changes in apparent membrane order as detected by steady-state fluorescence measurements, only ionophore treatment enhanced phospholipase activity. Experiments with exogenously-added phosphatidylserine indicated that the difference was not due to the presence of that anionic phospholipid in the outer membrane leaflet. Instead, analysis of the equilibration kinetics of various cationic membrane probes revealed that the difference could relate to the spacing of membrane lipids. Specifically, ionophore treatment increased that spacing while temperature only affected overall membrane order and fluidity. To consider the possibility that the distinction with ionophore might relate to the actin cytoskeleton, cells were stained with phalloidin and imaged via confocal microscopy. Ionophore caused disruption of actin fibers while increased temperature did not. This apparent connection between membrane hydrolysis and the cytoskeleton was further corroborated by examining the relationship among these events during apoptosis stimulated by thapsigargin.