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1.
In this work, high ΔμH+-dependent succinate oxidase activity has been demonstrated for the first time with membrane vesicles isolated from Bacillus subtilis. The maximal specific rate of succinate oxidation by coupled inside-out membrane vesicles isolated from a B. subtilis strain overproducing succinate:menaquinone oxidoreductase approaches the specific rate observed with the intact cells. Deenergization
of the membrane vesicles with ionophores or alamethicin brings about an almost complete inhibition of succinate oxidation.
An apparent K
m for succinate during the energy-dependent succinate oxidase activity of the vesicles (2.2 mM) is higher by an order of magnitude
than the K
m value measured for the energy-independent reduction of 2,6-dichlorophenol indophenol. The data reveal critical importance
of ΔμH+ for maintaining active electron transfer by succinate:menaquinone oxidoreductase. The role of ΔμH+ might consist in providing energy for thermodynamically unfavorable menaquinone reduction by succinate by virtue of transmembrane
electron transport within the enzyme down the electric field; alternatively, ΔμH+ could play a regulatory role by maintaining the electroneutrally operating enzyme in a catalytically active conformation. 相似文献
2.
The polyphasic patterns of fluorescence induction rise in pea leaves in vivo and after the treatment with ionophores have
been studied using a Plant Efficiency Analyzer. To analyze in detail photosystem II (PS II) electron transfer processes, an
extended PS II model was applied, which included the sums of exponential functions to specify explicitly the light-driven
formation of the transmembrane electric potential (ΔΨ(t)) as well as pH in the lumen (pHL(t)) and stroma (pHS(t)). PS II model parameters and numerical coefficients in ΔΨ(t), pHL(t), and pHS(t) were evaluated to fit fluorescence induction data for different experimental conditions: leaf in vivo or after ionophore
treatment at low or high light intensity. The model imitated changes in the pattern of fluorescence induction rise due to
the elimination of transmembrane potential in the presence of ionophores, when ΔΨ = 0 and pHL(t), pHS(t) changed to small extent relative to control values in vivo, with maximum ΔΨ(t) ∼ 90 mV and ΔΨ(t) ∼ 40 mV for the stationary state at ΔpH ≅ 1.8. As the light intensity was increased from 300 to 1200 μmol m−2 s−1, the heat dissipation rate constants increased threefold for nonradiative recombination of P680+Phe− and by ∼30% for P680+QA−. The parameters ΔΨ, pHS and pHL were analyzed as factors of PS II redox state populations and fluorescence yield. The kinetic mechanism of fluorescence quenching
is discussed, which is related with light-induced lumen acidification, when +QA− and P680+ recombination probability increases to regulate the QA reduction. 相似文献
3.
M. P. Fernandes N. M. Inada M. R. Chiaratti F. F. B. Araújo F. V. Meirelles M. T. S. Correia L. C. B. B. Coelho M. J. M. Alves F. R. Gadelha A. E. Vercesi 《Journal of bioenergetics and biomembranes》2010,42(1):69-78
Incubation of T. cruzi epimastigotes with the lectin Cramoll 1,4 in Ca2+ containing medium led to agglutination and inhibition of cell proliferation. The lectin (50 μg/ml) induced plasma membrane
permeabilization followed by Ca2+ influx and mitochondrial Ca2+ accumulation, a result that resembles the classical effect of digitonin. Cramoll 1,4 stimulated (five-fold) mitochondrial
reactive oxygen species (ROS) production, significantly decreased the electrical mitochondrial membrane potential (ΔΨm) and impaired ADP phosphorylation. The rate of uncoupled respiration in epimastigotes was not affected by Cramoll 1,4 plus
Ca2+ treatment, but oligomycin-induced resting respiration was 65% higher in treated cells than in controls. Experiments using
T. cruzi mitochondrial fractions showed that, in contrast to digitonin, the lectin significantly decreased ΔΨm by a mechanism sensitive to EGTA. In agreement with the results showing plasma membrane permeabilization and impairment of
oxidative phosphorylation by the lectin, fluorescence microscopy experiments using propidium iodide revealed that Cramoll
1,4 induced epimastigotes death by necrosis. 相似文献
4.
Water relations dynamics during simulated sunflecks at high (36°C) and medium (27°C) temperatures and high and low vapour
pressure deficits beween leaf and air (VPD) were studied on shade-grown Piper auritum H.B. & K. plants, a pioneer tree, common in gaps and clearings of tropical rain forests. The leaves of P. auritum wilt rapidly when exposed to high light. Exposure to high VPD and high light caused substantial and rapid dehydration of
leaves. Dehydration could be prevented under high humidity irrespective of temperature. Water stored in leaf cells served
as initial source for transpiration upon high light exposure. This effect increased with increasing VPD and temperature. The
pronounced decrease in leaf water content over time in high light caused a rapid decrease in leaf water potential (Ψl) and a concomitant increase in water potential gradient (ΔΨ/Δx) between trunk and leaf, yet the high leaf elasticity (small bulk elastic modulus, ε) allowed turgor maintenance under most
conditions. Under high VPD and high temperature, stomata remained open and ΔΨ/Δx frequently exceeded 0.95 MPa · m−1, the cavitation-inducing threshold (ΔΨ/Δx
cav) causing high rates of acoustic emissions from stems and leaf petioles and leading to concomitant losses in hydraulic conductance
per leaf area (k
l). At medium temperature (high VPD), stomatal closure contained xylem embolism by keeping ΔΨ/Δx at or below this threshold. We argue that wilting substantially contributes to creating a sufficient driving force for water
uptake from the soil, and reducing the VPD (through a decrease in radiation load and thus leaf temperature) to avoid excessive
dehydration.
Received: 3 March 1996 / Accepted: 10 November 1996 相似文献
5.
Among other mitochondrial functions, energy production and Ca2+ uptake are crucial for maintaining neuronal viability. Both of these functions are critically dependent on mitochondrial
membrane potential (ΔΨm). Mitochondrial Ca2+ overload causing a dissipation of ΔΨm is a key component of several neuronal pathologies. However, the mechanism of Ca2+-induced depolarization in neuronal mitochondria remains unclear. Typically, ΔΨm has been evaluated as a single overall estimate from all mitochondria present in a given cell or tissue. However, recent
data showed that the population of mitochondria isolated from tissues is not homogeneous, and averaged parameters from the
whole population do not necessarily reflect the processes taking place in a single organelle. This review summarizes our recent
studies of Ca2+-induced depolarization in individual mitochondria isolated from rat forebrain and immobilized to coverslips. Fluorescence
imaging techniques and potentiometric fluorescent dyes were effectively used to study ΔΨm changes. The data have shown that Ca2+ triggers ΔΨm oscillations in brain mitochondria followed by a complete depolarization. Further investigation of this phenomenon led us
to suggest that Ca2+-induced ΔΨm oscillations can represent an intermediate unstable state that may lead to irreversible mitochondrial dysfunction. Therefore,
further study of this phenomenon would help to understand what causes the irreversible damage of mitochondria during cytosolic/mitochondrial
Ca2+ overload. Here we discuss the effects of different modulators of the mitochondrial permeability transition pore on Ca2+-induced depolarization in brain mitochondria and in liver mitochondria, where the mechanism of Ca2+-depolarization is better understood. A comparison of these effects in brain and liver mitochondria led us to conclude that
Ca2+ can induce reversible “low conductance” permeability transition in brain mitochondria, the phenomenon which requires a transient
conformational change of the adenine nucleotide translocator from a specific transporter to a non-specific pore.
The article is published in the original. 相似文献
6.
Characean internodal cells generate receptor potential (ΔE
m) in response to mechanical stimuli. Upon a long-lasting stimulus, the cells generated ΔE
m at the moment of both compression and decompression, and the amplitude of ΔE
m at the moment of decompression, (ΔE
m)E, was larger than that at compression. The long-lasting stimulus caused a membrane deformation (ΔD
m) having two components, a rapid one, (ΔD
m)rapid, at the moment of compression and a slower one, (ΔD
m)slow, during the long-lasting compression. We assumed that (ΔD
m)slow might have some causal relation with the larger ΔE
m at (ΔE
m)E. We treated internodal cells with either HgCl2 or ZnCl2, water channel inhibitors, to decrease (ΔD
m)slow. Both inhibitors attenuated (ΔD
m)slow during compression. Cells treated with HgCl2 generated smaller (ΔE
m)E compared to nontreated cells. On the other hand, cells treated with ZnCl2 never attenuated (ΔE
m)E but, rather, amplified it. Thus, the amplitude of (ΔD
m)slow did not always show tight correlation with the amplitude of (ΔE
m)E. Furthermore, when a constant deformation was applied to an internodal cell in a medium with higher or lower osmotic value,
a cell having higher turgor always showed a larger (ΔE
m)E. Thus, we concluded that changes in tension at the membrane may be the most important factor to induce activation of mechanosensitive
Ca2+ channel. 相似文献
7.
Homocysteine affects cardiomyocyte viability: concentration-dependent effects on reversible flip-flop, apoptosis and necrosis 总被引:1,自引:0,他引:1
Sipkens JA Krijnen PA Meischl C Cillessen SA Smulders YM Smith DE Giroth CP Spreeuwenberg MD Musters RJ Muller A Jakobs C Roos D Stehouwer CD Rauwerda JA van Hinsbergh VW Niessen HW 《Apoptosis : an international journal on programmed cell death》2007,12(8):1407-1418
Background Hyperhomocysteinaemia (HHC) is thought to be a risk factor for cardiovascular disease including heart failure. While numerous
studies have analyzed the role of homocysteine (Hcy) in the vasculature, only a few studies investigated the role of Hcy in
the heart. Therefore we have analyzed the effects of Hcy on isolated cardiomyocytes.
Methods H9c2 cells (rat cardiomyoblast cells) and adult rat cardiomyocytes were incubated with Hcy and were analyzed for cell viability.
Furthermore, we determined the effects of Hcy on intracellular mediators related to cell viability in cardiomyocytes, namely
NOX2, reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨ
m) and ATP concentrations.
Results We found that incubation of H9c2 cells with 0.1 mM D,L-Hcy (= 60 μM l-Hcy) resulted in an increase of ΔΨ
m as well as ATP concentrations. 1.1 mM d,l-Hcy (= 460 μM l-Hcy) induced reversible flip-flop of the plasma membrane phospholipids, but not apoptosis. Incubation with 2.73 mM d,l-Hcy (= 1.18 mM l-Hcy) induced apoptosis and necrosis. This loss of cell viability was accompanied by a thread-to-grain transition of the mitochondrial
reticulum, ATP depletion and nuclear NOX2 expression coinciding with ROS production as evident from the presence of nitrotyrosin
residues. Notably, only at this concentration we found a significant increase in S-adenosylhomocysteine which is considered
the primary culprit in HHC.
Conclusion We found concentration-dependent effects of Hcy in cardiomyocytes, varying from induction of reversible flip-flop of the plasma
membrane phospholipids, to apoptosis and necrosis. 相似文献
8.
Propyl gallate (PG) as a synthetic antioxidant exerts a variety of effects on tissue and cell functions. Here, we investigated
the effects of MAPK (MEK, JNK and p38) inhibitors on PG-treated HeLa cells in relation to cell death, ROS and GSH levels.
PG induced cell growth inhibition and apoptosis in HeLa cells, which was accompanied by the loss of mitochondrial membrane
potential (MMP; ΔΨm). ROS levels were increased or decreased in PG-treated HeLa cells depending on the incubation times. PG also increased GSH
depleted cell numbers in HeLa cells. All the MAPK inhibitors slightly enhanced cell growth inhibition, death and MMP (ΔΨm) loss, and increased ROS levels in PG-treated HeLa cells. However, MAPK inhibitors did not significantly affect GSH depletion
in PG-treated cells. In conclusion, the enhanced effect of MAPK inhibitors on PG-induced HeLa cell death was accompanied by
increasing ROS levels but the effect was not related to changes of GSH level. 相似文献
9.
Y. R. Abdrakhimova I. M. Andreev A. G. Shugaev 《Russian Journal of Plant Physiology》2011,58(4):567-574
Effects of cyanide-resistant alternative oxidase (AOX) and modulators of plant uncoupling mitochondrial proteins (PUMP) on
respiration rate and generation of transmembrane electric potential (ΔΨ) were investigated during oxidation of various substrates
by isolated mitochondria from etiolated coleoptiles of winter wheat (Triticum aestivum L.). Oxidative phosphorylation in wheat mitochondria during malate and succinate oxidation was quite effective (it was characterized
by high respiratory control ratio as defined by Chance, high ADP/O ratio, and rapid ATP synthesis). Nevertheless, the effectiveness
of oxidative phosphorylation was substantially modulated by operation of energy-dissipating systems. The application of safranin
dye revealed the partial dissipation of ΔΨ during inhibition of cytochrome-mediated malate oxidation by cyanide and antimycin
A and demonstrated the operation of AOX-dependent compensatory mechanism for ΔΨ generation. The complex I of mitochondrial
electron transport chain was shown to play the dominant role in ΔΨ generation and ATP synthesis during AOX functioning upon
inhibition of electron transport through the cytochrome pathway. Effects of linoleic acid (PUMP activator) at physiologically
low concentrations (4–10 μM) on respiration and ΔΨ generation in mitochondria were examined. The uncoupling effect of linoleic
acid was shown in activation of the State 4 respiration, as well as in ΔΨ dissipation; this effect was eliminated in the presence
of BSA but was insensitive to purine nucleotides. The uncoupling effect of linoleic acid was accompanied by reversible inhibition
of AOX activity. The results are discussed with regard to possible physiological role of mitochondrial energy-dissipating
systems in regulation of energy transduction in plant cells under stress conditions. 相似文献
10.
Arsenic trioxide (ATO; As2O3) can induce apoptotic cell death in various cancer cells including lung cancer cells. However, little is known about the
toxicological effects of ATO on normal primary lung cells. In this study, we investigated the cellular effects of ATO on human
pulmonary fibroblast (HPF) cells in relation to cell growth inhibition and death. ATO inhibited HPF cell growth with an IC50 of approximately 30–40 μM at 24 h and induced cell death accompanied by the loss of mitochondrial membrane potential (MMP;
ΔΨm). Thus, HPF cells were considered to be very resistant to ATO insults. ATO increased the expression of p53 protein and decreased
that of Bcl-2 protein. This agent activated caspase-8 but not caspase-3 in HPF cells. Z-VAD (a pan-caspase inhibitor; 15 μM)
did not significantly decrease cell growth inhibition, death and MMP (ΔΨm) loss by ATO. Moreover, administration of Bax or casase-8 siRNA attenuated HPF cell death by ATO whereas p53 or caspase-3
siRNAs did not affect cell death. In conclusion, HPF cells were resistant to ATO and higher doses of ATO induced the growth
inhibition and death in HPF cells via the regulation of Bcl-2 family and caspase-8. 相似文献
11.
Toshiyuki Kaneko Naoya Takahashi Munehiro Kikuyama 《The Journal of membrane biology》2009,228(1):33-42
In order to confirm that mechanosensitive Ca2+ channels are activated by membrane stretching, we stretched or compressed the plasma membrane of Chara by applying osmotic shrinkage or swelling of the cell by varying the osmotic potential of the bathing medium. Aequorin studies
revealed that treatments causing membrane stretching induced a transient but large increase in cytoplasmic concentration of
Ca2+ (Δ[Ca2+]c). However, the observed Δ[Ca2+]c decreased during the treatments, resulting in membrane compression. A second experiment was carried out to study the relationship
between changes in membrane potential (ΔE
m) and stretching or compression of the plasma membrane. Significant ΔE
m values, often accompanied by an action potential, were observed during the initial exchange of the bathing medium from a
hypotonic medium to a hypertonic one (plasmolysis). ΔE
m appears to be triggered by a partial stretching of the membrane as it was peeled from the cell wall. After plasmolysis, other
exchanges from hypertonic to hypotonic media, with their accompanying membrane stretching, always induced large ΔE
m values and were often accompanied by an action potential. By contrast, action potentials were scarcely observed during other
exchanges from hypotonic to hypertonic solutions (=membrane compression). Thus, we concluded that activation of the mechanosensitive
channels is triggered by membrane stretching in Chara. 相似文献
12.
Photoinhibition of colonial and unicellular <Emphasis Type="Italic">Microcystis</Emphasis> cells in a summer bloom in Lake Taihu 总被引:1,自引:0,他引:1
To evaluate the photoinhibition of colonial and unicellular cells of Microcystis aeruginosa under natural conditions, the maximum and effective quantum yields of photosystem II were measured from variable chlorophyll
a fluorescence in samples from Lake Taihu during a summer bloom from June 19 to 21, 2006. Diurnal changes in the photoinhibition
of Microcystis cells incubated immediately below the surface in clear bottles for 30 min and in situ samples under natural conditions were
measured. At solar noon during the three days, the mean values of maximum quantum yield (F
v/F
m) and effective quantum yield (ΔF/F
m′) for unicellular cells (F
v/F
m = 0.15, ΔF/F
m′ = 0.10) were lower than those for colonial cells (F
v/F
m = 0.25, ΔF/F
m′ = 0.15). For in situ samples, the values of F
v/F
m and ΔF/F
m′ for colonial cells at solar noon on the three days (F
v/F
m 0.30, 0.25, 0.29; ΔF/F
m′ 0.24, 0.21, 0.22) were also higher than those of unicellular cells (F
v/F
m 0.26, 0.18, 0.25; ΔF/F
m′ 0.15, 0.11, 0.14). The results indicate that colony formation has a protective effect on Microcystis cells by reducing the occurrence of photoinhibition under high light intensities. 相似文献
13.
Lasfer M Vadrot N Aoudjehane L Conti F Bringuier AF Feldmann G Reyl-Desmars F 《Cell biology and toxicology》2008,24(1):55-62
The heavy metal cadmium, an environmental pollutant, has been widely demonstrated to be toxic, in particular for liver. In
murines, cadmium induces apoptosis of hepatocytes and hepatomas. In human cells, apoptosis induced by cadmium has been exclusively
demonstrated in tumoral cell lines. Nothing was known in normal liver, in vitro or in vivo. In the present study, we examined the effects of cadmium in nonmalignant human hepatocytes. For that purpose, we investigated
whether cadmium was able to induce apoptosis of normal human hepatocytes (NHH) in primary culture and of a SV40-immortalized
human hepatocyte (IHH) cell line. Treatment of IHH and NHH with cadmium induced the presence of a sub-G1 population at 10 and 100 μmol/L, respectively. DAPI staining of both cell types treated with cadmium 100 μmol/L revealed
the induction of nuclear apoptotic bodies, supporting the hypothesis of apoptosis. In IHH and NHH, cadmium 100 μmol/L induced
PARP cleavage into a 85 kDa fragment. In order to investigate the involvement of mitochondria in cadmium-induced apoptosis,
we measured the mitochondrial membrane potential (ΔΨm). We observed that in IHH and NHH, cadmium 100 μmol/L induced a decrease of ΔΨm. As expected, cadmium under the same conditions enhanced caspase-9 and caspase-3 activities. In addition, cadmium from 1
to 100 μmol/L induced the expression of p53 and phosphorylation of its Ser15 in IHH and NHH. In conclusion, we showed in this
study that human hepatocytes were sensitive to cadmium and apoptosis induced at concentrations suggested in the literature
to inhibit p53 DNA-binding and DNA repair. 相似文献
14.
Stomatal conductance (g
s) and transpiration rates vary widely across plant species. Leaf hydraulic conductance (k
leaf) tends to change with g
s, to maintain hydraulic homeostasis and prevent wide and potentially harmful fluctuations in transpiration-induced water potential
gradients across the leaf (ΔΨ
leaf). Because arbuscular mycorrhizal (AM) symbiosis often increases g
s in the plant host, we tested whether the symbiosis affects leaf hydraulic homeostasis. Specifically, we tested whether k
leaf changes with g
s to maintain ΔΨ
leaf or whether ΔΨ
leaf differs when g
s differs in AM and non-AM plants. Colonization of squash plants with Glomus intraradices resulted in increased g
s relative to non-AM controls, by an average of 27% under amply watered, unstressed conditions. Stomatal conductance was similar
in AM and non-AM plants with exposure to NaCl stress. Across all AM and NaCl treatments, k
leaf did change in synchrony with g
s (positive correlation of g
s and k
leaf), corroborating leaf tendency toward hydraulic homeostasis under varying rates of transpirational water loss. However, k
leaf did not increase in AM plants to compensate for the higher g
s of unstressed AM plants relative to non-AM plants. Consequently, ΔΨ
leaf did tend to be higher in AM leaves. A trend toward slightly higher ΔΨ
leaf has been observed recently in more highly evolved plant taxa having higher productivity. Higher ΔΨ
leaf in leaves of mycorrhizal plants would therefore be consistent with the higher rates of gas exchange that often accompany
mycorrhizal symbiosis and that are presumed to be necessary to supply the carbon needs of the fungal symbiont. 相似文献
15.
16.
Membrane electroporation, vesicle shape deformation and aggregation of small, NaCl-filled lipid vesicles (of radius a = 50
nm) in DC electric fields was characterized using conductometric and turbidimetrical data. At pulse durations tE≤ 55 ± 5 ms the increase in the conductivity of the vesicle suspension is due to the field-induced efflux of electrolyte through
membrane electropores. Membrane electroporation and Maxwell stress on the vesicle membrane lead to vesicle elongation concomitant
with small volume reduction (up to 0.6% in an electric field of E = 1 MV m–1). At tE > 55 ± 5 ms, further increases in the conductivity and the optical density suggest electroaggregation and electrofusion of
vesicles. The conductivity changes after the electric pulse termination reflect salt ion efflux through slowly resealing electropores.
The analysis of the volume reduction kinetics yields the bending rigidity κ = (4.1 ± 0.3) ⋅ 10–20 J of the vesicle membrane. If the flow of Na+ and Cl– ions from the vesicle interior is treated in terms of Hagen-Poiseuille's equation, the number of permeable electropores is
N = 39 per vesicle with mean pore radius rp = 0.85 ± 0.05 nm at E = 1 MVm–1 and tE≤ 55 ± 5 ms. The turbidimetric and conductometric data suggest that small lipid vesicles (a ≤ 50 nm) are not associated with extensive membrane thermal undulations or superstructures. In particular
with respect to membrane curvature, the vesicle results are suggestive for the design and optimization of electroporative
delivery of drugs and genes to cell tissue at small field strengths (≤1 MVm–1) and large pulse durations (≤100 ms).
Received: 8 July 1997 / Accepted: 15 September 1997 相似文献
17.
Galluzzi L Zamzami N de La Motte Rouge T Lemaire C Brenner C Kroemer G 《Apoptosis : an international journal on programmed cell death》2007,12(5):803-813
Mitochondrial membrane permeabilization (MMP) is considered as the “point-of-no-return” in numerous models of programmed cell
death. Indeed, mitochondria determine the intrinsic pathway of apoptosis, and play a major role in the extrinsic route as
well. MMP affects the inner and outer mitochondrial membranes (IM and OM, respectively) to a variable degree. OM permeabilization
culminates in the release of proteins that normally are confined in the mitochondrial intermembrane space (IMS), including
caspase activators (e.g. cytochrome c) and caspase-independent death effectors (e.g. apoptosis-inducing factor). Partial IM permeabilization disrupts mitochondrial ion and volume homeostasis and dissipates
the mitochondrial transmembrane potential (ΔΨm). The assessment of early mitochondrial alterations allows for the identification of cells that are committed to die but
have not displayed yet the apoptotic phenotype. Several techniques to measure MMP by cytofluorometry and fluorescence microscopy
have been developed. Here, we summarize the currently available methods for the detection of MMP, and provide a comparative
analysis of these techniques. 相似文献
18.
A. G. Shugaev N. A. Shugaeva D. A. Lashtabega E. I. Vyskrebentseva 《Russian Journal of Plant Physiology》2010,57(2):189-197
The effect of substitution of KCl for sucrose in the reaction medium on succinate oxidation and hydrogen peroxide generation
was investigated in the mitochondria isolated from stored taproots of sugar beet (Beta vulgaris L.). In a sucrose-containing medium, oxidation of succinate was inhibited by oxaloacetate; this inhibition was especially
pronounced upon a decrease in substrate concentration and eliminated in the presence of glutamate, which removed oxaloacetate
in the course of transamination. Irrespective of succinate concentration, substitution of KCl for sucrose in the medium considerably
enhanced suppression of succinate oxidation apparently as a result of slow activation of succinate dehydrogenase (SDH) by
its substrate. In this case, mitochondria showed the symptoms of uncoupling, lower values of membrane potential (ΔΨ), respiratory
control (RC), and ADP/O induced by electrophoretic transport of potassium via K+ channel of mitochondria. KCl-dependent suppression of succinate oxidation by taproot mitochondria was accompanied by a considerable
inhibition of H2O2 production as compared with the sucrose-containing medium. These results indicate that in the presence of potassium ions,
ΔΨ dissipates, suppression of succinate oxidation by oxaloacetate increases, and succinate-dependent generation of ROS in
sugar beet mitochondria is inhibited. A possible physiological role of oxaloacetate-restricted SDH activity in the suppression
of respiration of storage organs protecting mitochondria from oxidative stress is discussed. 相似文献
19.
Predawn disequilibrium between plant and soil water potentials in two cold-desert shrubs 总被引:15,自引:0,他引:15
L. A. Donovan D. J. Grisé J. B. West R. A. Pappert N. N. Alder J. H. Richards 《Oecologia》1999,120(2):209-217
Classical water relations theory predicts that predawn plant water potential should be in equilibrium with soil water potential
(soil Ψw) around roots, and many interpretations of plant water status in natural populations are based on this expectation. We examined
this expectation for two salt-tolerant, cold-desert shrub species in glasshouse experiments where frequent watering assured
homogeneity in soil Ψw and soil-root hydraulic continuity and where NaCl controlled soil Ψw. Plant water potentials were measured with a pressure chamber (xylem Ψp) and thermocouple psychrometers (leaf Ψw). Soil Ψw was measured with in situ thermocouple psychrometers. Predawn leaf Ψw and xylem Ψp were significantly more negative than soil Ψw, for many treatments, indicating large predawn soil-plant Ψw disequilibria: up to 1.2 MPa for Chrysothamnus nauseosus (0 and 100 mm NaCl) and 1.8 MPa for Sarcobatus vermiculatus (0, 100, 300, and 600 mm NaCl). Significant nighttime canopy water loss was one mechanism contributing to predawn disequilibrium, assessed by comparison
of xylem Ψp for bagged (to minimize transpiration) and unbagged canopies, and by gas exchange measurements. However, nighttime transpiration
accounted for only part of the predawn disequilibrium. Other mechanisms that could act with nighttime transpiration to generate
large predawn disequilibria are described and include a model of how leaf apoplastic solutes could contribute to the phenomenon.
This study is among the first to conclusively document such large departures from the expectation of predawn soil-plant equilibrium
for C3 shrubs, and provides a general framework for considering relative contributions of nighttime transpiration and other plant-related
mechanisms to predawn disequilibrium.
Received: 12 November 1998 / Accepted: 5 May 1999 相似文献
20.
By simultaneously analyzing the chlorophyll a fluorescence transient and light absorbance at 820 nm as well as chlorophyll fluorescence quenching, we investigated the
effects of different photon flux densities (0, 15, 200 μmol m−2 s−1) with or without 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) on the repair process of cucumber (Cucumis sativus L.) leaves after treatment with low temperature (6°C) combined with moderate photon flux density (200 μmol m−2 s−1) for 6 h. Both the maximal photochemical efficiency of Photosystem II (PSII) (F
v/F
m) and the content of active P700 (ΔI/I
o) significantly decreased after chilling treatment under 200 μmol m−2 s−1 light. After the leaves were transferred to 25°C, F
v/F
m recovered quickly under both 200 and 15 μmol m−2 s−1 light. ΔI/I
o recovered quickly under 15 μmol m−2 s−1 light, but the recovery rate of ΔI/I
o was slower than that of F
v/F
m. The cyclic electron transport was inhibited by chilling-light treatment obviously. The recovery of ΔI/I
o was severely suppressed by 200 μmol m−2 s−1 light, whereas a pretreatment with DCMU effectively relieved this suppression. The cyclic electron transport around PSI recovered
in a similar way as the active P700 content did, and the recovery of them was both accelerated by pretreatment with DCMU.
The results indicate that limiting electron transport from PSII to PSI protected PSI from further photoinhibition, accelerating
the recovery of PSI. Under a given photon flux density, faster recovery of PSII compared to PSI was detrimental to the recovery
of PSI or even to the whole photosystem. 相似文献