Relevant bibliographies by topics / Cell respiration

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cell respiration'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 January 2023

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Journal articles on the topic "Cell respiration"

1

Harborne, Jeffrey B. "Higher plant cell respiration." Phytochemistry 25, no. 6 (May 1986): 1515. http://dx.doi.org/10.1016/s0031-9422(00)81331-x.

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Black, Clanton C. "Plant Respiration Higher Plant Cell Respiration R. Douce D. A. Day." BioScience 37, no. 10 (November 1987): 742–43. http://dx.doi.org/10.2307/1310486.

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Li, Ding, Zhexu Ding, Manjin Gui, Yanmei Hou, and Kui Xie. "Metabolic Enhancement of Glycolysis and Mitochondrial Respiration Are Essential for Neuronal Differentiation." Cellular Reprogramming 22, no. 6 (December 1, 2020): 291–99. http://dx.doi.org/10.1089/cell.2020.0034.

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Garmash, E. V. "Mitochondrial respiration of the photosynthesizing cell." Russian Journal of Plant Physiology 63, no. 1 (January 2016): 13–25. http://dx.doi.org/10.1134/s1021443715060072.

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SIEDOW, J. N. "Plant Mitochondria: Higher Plant Cell Respiration." Science 230, no. 4723 (October 18, 1985): 313–14. http://dx.doi.org/10.1126/science.230.4723.313.

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Mawson, B. T. "Cyanide-resistant, alternative pathway respiration in guard cell protoplasts of Vicia faba." Canadian Journal of Botany 72, no. 2 (February 1, 1994): 150–56. http://dx.doi.org/10.1139/b94-020.

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The activity and capacity of cyanide-resistant or alternative pathway respiration was examined in Vicia faba L. guard and mesophyll cell protoplasts maintained either in darkness (dark adapted) or illuminated with blue light. Respiration rates by dark-adapted guard cell protoplasts were unaffected by titrating with salicylhydroxamic acid (0.1–2.0 mM), an inhibitor of alternative pathway respiration, suggesting the lack of activity of this pathway. In combination with 0.1 mM KCN, an inhibitor of cytochrome pathway respiration, salicylhydroxamic acid was effective in inhibiting total respiration rates. In contrast with guard cell protoplasts, salicylhydroxamic acid reduced rates of O2 consumption in dark-adapted mesophyll cell protoplasts by 25–30% of total respiration. Titrating the cytochrome pathway of guard cell protoplasts with KCN (10–140 μM) alone failed to reduce respiratory activity but was effective in combination with salicylhydroxamic acid. Addition of a proton ionophore, carbonyl cyanide m-chlorophenylhydraxone, to dark-adapted guard cell protoplast suspensions increased respiration by approximately 30 and 84% in the presence and absence of salicylhydroxamic acid, suggesting restriction of electron flow by adenylates. Illumination of guard cell protoplasts with blue light for 30 min increased the sensitivity of respiration to salicylhydroxamic acid and increased the activity of the alternative pathway over this time period to ~55% of total respiration. Blue light also increased the rate of uncoupled respiration by guard cell protoplasts treated with salicylhydroxamic acid compared with dark-adapted protoplasts. The results suggest that electron movement through either cytochrome or alternative pathways in guard cell mitochondria may be regulated during signal transduction of blue light. Key words: Vicia faba, guard cell protoplasts, alternative pathway, respiration, blue light.
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MacDonald, J. R., M. Oellermann, S. Rynbeck, G. Chang, K. Ruggiero, G. J. S. Cooper, and A. J. R. Hickey. "Transmural differences in respiratory capacity across the rat left ventricle in health, aging, and streptozotocin-induced diabetes mellitus: evidence that mitochondrial dysfunction begins in the subepicardium." American Journal of Physiology-Cell Physiology 300, no. 2 (February 2011): C246—C255. http://dx.doi.org/10.1152/ajpcell.00294.2010.

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In diabetic cardiomyopathy, ventricular dysfunction occurs in the absence of hypertension or atherosclerosis and is accompanied by altered myocardial substrate utilization and depressed mitochondrial respiration. It is not known if mitochondrial function differs across the left ventricular (LV) wall in diabetes. In the healthy heart, the inner subendocardial region demonstrates higher rates of blood flow, oxygen consumption, and ATP turnover compared with the outer subepicardial region, but published transmural respirometric measurements have not demonstrated differences. We aim to measure mitochondrial function in Wistar rat LV to determine the effects of age, streptozotocin-diabetes, and LV layer. High-resolution respirometry measured indexes of respiration in saponin-skinned fibers dissected from the LV subendocardium and subepicardium of 3-mo-old rats after 1 mo of streptozotocin-induced diabetes and 4-mo-old rats following 2 mo of diabetes. Heart rate and heartbeat duration were measured under isoflurane-anesthesia using a fetal-Doppler, and transmission electron microscopy was employed to observe ultrastructural differences. Heart rate decreased with age and diabetes, whereas heartbeat duration increased with diabetes. While there were no transmural respirational differences in young healthy rat hearts, both myocardial layers showed a respiratory depression with age (30–40%). In 1-mo diabetic rat hearts only subepicardial respiration was depressed, whereas after 2 mo diabetes, respiration in subendocardial and subepicardial layers was depressed and showed elevated leak (state 2) respiration. These data provide evidence that mitochondrial dysfunction is first detectable in the subepicardium of diabetic rat LV, whereas there are measureable changes in LV mitochondria after only 4 mo of aging.
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Alfatni, Abrar, Anne-Laure Charles, François Sauer, Marianne Riou, Fabienne Goupilleau, Samy Talha, Alain Meyer, et al. "Peripheral Blood Mononuclear Cells Mitochondrial Respiration and Superoxide Anion after Heart Transplantation." Journal of Clinical Medicine 11, no. 23 (December 6, 2022): 7247. http://dx.doi.org/10.3390/jcm11237247.

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Introduction: The mitochondrial function of circulating peripheral blood mononuclear cells (PBMCs) is an interesting new approach to cardiac diseases. Thus, PBMC’s mitochondrial respiration decreases in relation to heart failure severity. However, no data are available on heart-transplanted patients (Htx). Population and Methods: We determined PBMCs mitochondrial respiration by high-resolution respirometry (Oroboros Instruments) and superoxide anion production using electron paramagnetic resonance (Bruker-Biospin) in 20 healthy subjects and 20 matched Htx and investigated clinical, biological, echocardiographic, coronarography and biopsy characteristics. Results: PBMCs mitochondrial respiratory chain complex II respiration was decreased in Htx (4.69 ± 0.84 vs. 7.69 ± 1.00 pmol/s/million cell in controls and Htx patients, respectively; p = 0.007) and complex IV respiration was increased (24.58 ± 2.57 vs. 15.68 ± 1.67 pmol/s/million cell; p = 0.0035). Superoxide anion production was also increased in Htx (1.47 ± 0.10 vs. 1.15 ± 0.10 µmol/min; p = 0.041). The leucocyte-to-lymphocyte ratio was increased in Htx, whom complex II correlated with leucocyte number (r = 0.51, p = 0.02) and with the left ventricular posterior wall peak early diastolic myocardial velocity (r = −0.62, p = 0.005). Complex IV was increased in the two patients with acute rejection and correlated negatively with Htx’s isovolumetric relation time (r = −0.45, p = 0.045). Discussion: Although presenting with normal systolic function, Htx demonstrated abnormal PBMC’s mitochondrial respiration. Unlike immunosuppressive therapies, subclinical diastolic dysfunction might be involved in these changes. Additionally, lymphopenia might reduce complex II, and acute rejection enhances complex IV respirations. Conclusion: PBMC’s mitochondrial respiration appears modified in Htx, potentially linked to cellular shift, mild diastolic dysfunction and/or acute rejection.
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Owiredu, Shawn, Abhay Ranganathan, David M. Eckmann, Frances S. Shofer, Kevin Hardy, David S. Lambert, Matthew Kelly, and David H. Jang. "Ex vivo use of cell-permeable succinate prodrug attenuates mitochondrial dysfunction in blood cells obtained from carbon monoxide-poisoned individuals." American Journal of Physiology-Cell Physiology 319, no. 1 (July 1, 2020): C129—C135. http://dx.doi.org/10.1152/ajpcell.00539.2019.

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The purpose of this study was to evaluate a new pharmacological strategy using a first-generation succinate prodrug, NV118, in peripheral blood mononuclear cells (PBMCs) obtained from subjects with carbon monoxide (CO) poisoning and healthy controls. We obtained human blood cells from subjects with CO poisoning and healthy control subjects. Intact PBMCs from subjects in the CO and Control group were analyzed with high-resolution respirometry measured in pmol O2 per second per 10−6 PBMCs. In addition to obtaining baseline respiration, NV118 (100 μM) was injected, and the same parameters of respiration were obtained for comparison in PBMCs. We measured mitochondrial dynamics with microscopy with the same conditions. We enrolled 37 patients (17 in the CO group and 20 in the Control group for comparison) in the study. PMBCs obtained from subjects in the CO group had overall significantly lower respiration compared with the Control group ( P < 0.0001). There was a significant increase in respiration with NV118, specifically with an increase in maximum respiration and respiration from complex II and complex IV ( P < 0.0001). The mitochondria in PBMCs demonstrated an overall increase in net movement compared with the Control group. Our results of this study suggest that the therapeutic compound, NV118, increases respiration at complex II and IV as well as restoration of mitochondrial movement in PBMCs obtained from subjects with CO poisoning. Mitochondrial-directed therapy offers a potential future strategy with further exploration in vivo.
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Nowak, Grazyna, and Diana Bakajsova. "Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells." American Journal of Physiology-Renal Physiology 303, no. 4 (August 15, 2012): F515—F526. http://dx.doi.org/10.1152/ajprenal.00072.2012.

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We demonstrated that nonselective PKC activation promotes mitochondrial function in renal proximal tubular cells (RPTC) following toxicant injury. However, the specific PKC isozyme mediating this effect is unknown. This study investigated the role of PKC-α in the recovery of mitochondrial functions in oxidant-injured RPTC. Wild-type PKC-α (wtPKC-α) and inactive PKC-α mutants were overexpressed in RPTC to selectively increase or block PKC-α activation. Oxidant ( tert-butyl hydroperoxidel; TBHP) exposure activated PKC-α in RPTC but decreased PKC-α levels in mitochondria following treatment. Uncoupled and state 3 respirations and activities of complexes I and IV in TBHP-injured cells decreased to 55, 44, 49, and 65% of controls, respectively. F0F1-ATPase activity and ATP content in injured RPTC decreased to 59 and 60% of controls, respectively. Oxidant exposure increased reactive oxygen species (ROS) production by 210% and induced mitochondrial fragmentation and 52% RPTC lysis. Overexpressing wtPKC-α did not block TBHP-induced ROS production but improved respiration and complex I activity, restored complex IV and F0F1-ATPase activities, promoted recovery of ATP content, blocked mitochondrial fragmentation, and reduced RPTC lysis to 14%. In contrast, inhibiting PKC-α 1) induced mitochondrial hyperpolarization and fragmentation; 2) blocked increases in ROS production; 3) prevented recovery of respiratory complexes and F0F1-ATPase activities, respiration, and ATP content; and 4) exacerbated TBHP-induced RPTC lysis. We conclude that 1) activation of PKC-α prevents mitochondrial hyperpolarization and fragmentation, decreases cell death, and promotes recovery of mitochondrial respiration and ATP content following oxidant injury in RPTC; and 2) respiratory complexes I and IV and F0F1-ATPase are targets of active PKC-α.
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Dissertations / Theses on the topic "Cell respiration"

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Fengler, John Josef Paul. "Respiration induced oxygen gradients in cultured mammalian cells." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28381.

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Oxygen is known to sensitize X-irradiated cells to lethal radiation damage. At low ambient oxygen tensions, however, the molecular mechanisms of the sensitization process and the metabolic requirements of the cell may be forced to compete for the cellular oxygen supply. The effect of cell respiration on the availability of intracellular oxygen during irradiation was consequently investigated by comparing the radiosensitivities of respiring and non-respiring cells. Cultured mammalian cells were irradiated in single cell suspensions and thin film monolayers at respiration inhibiting (4°C) and at normal cell culturing (37°C) temperatures. Due to oxygen equilibration and radiolytic depletion problems, the results of the suspension culture experiments were inconclusive. By subsequently analyzing the diffusive mass transfer of oxygen in the suspension medium, the stirrer flask was determined to be an inappropriate culture vessel in which to irradiate cells at constant low oxygen concentrations. A thin film cell culture system in which the oxygen concentrations to which the cells were exposed during irradiation could be more accurately controlled was then developed. A comparison of the oxygen enhanced radiosensitivities of the respiring and non-respiring cells in thin film monolayers suggested that the metabolic depletion of oxygen at low oxygen tensions has a significant effect on the local and intracellular oxygen distribution. These effects are representative of those that would be produced if respiration induced oxygen gradients existed inside and immediately around respiring cells. The magnitude of the differential radiosensitivities was found to be dependent on cell shape and to have values that agreed very well with theoretical predictions based on the existence of such gradients.
Science, Faculty of
Physics and Astronomy, Department of
Graduate
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Gui, Dan Y. (Dan Yi). "The role of respiration in supporting cell proliferation." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/115451.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, June 2017.
Cataloged from PDF version of thesis. "May 2017." Page 163 blank. Vita.
Includes bibliographical references.
Compared to non-proliferating cells, proliferating cells such as cancer cells have additional metabolic requirements for generating biomass. However, despite these additional requirements the components of the mammalian metabolic network in both proliferating and non-proliferating cells are largely the same. Thus, in order to balance the competing anabolic and catabolic needs of a proliferating cell, the same metabolic networks components must take on distinct roles. Understanding how the various network components support proliferation may lead to improvements in cancer therapy. It has long been known that mitochondrial respiration is essential for proliferation. However, the precise metabolic role that is filled by respiration is not well defined. This thesis focuses on understanding the role of respiration in supporting mammalian proliferation. In non-proliferating cells respiration is considered to be primarily an ATP-producing catabolic process. We find that in proliferating cells, respiration serves a crucial anabolic role by providing access to an electron acceptor in the form of molecular oxygen. Electron acceptor availability is required for maintaining NAD+/NADH homeostasis and supporting aspartate synthesis. In conditions where alternative electron acceptors are provided such that cells can maintain NAD+/NADH homeostasis through alternative pathways, or when exogenous aspartate is provided, respiration is dispensable for proliferation. These findings highlight that metabolic dependencies can be modified by environmental conditions. Consistent with this, we find that altering NAD+/NADH homeostasis through alternative pathways or providing exogenous aspartate can modulate cellular sensitivity to respiration inhibitors such as metformin. Collectively, these studies contribute to an understanding of how metabolism supports biomass generation for proliferation and offers insight to how metabolism could be targeted for cancer therapy.
by Dan Y. Gui.
Ph. D.
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Tippetts, Trevor Stanley. "Cigarette Smoke Increases Cardiomyocyte Ceramide Accumulation and Inhibits Mitochondrial Respiration." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/5596.

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Cigarette smoking is a common and lethal worldwide habit, with considerable mortality stemming from its deleterious effects on heart function. While current theories posit altered blood lipids and fibrinogen metabolism as likely mediators, none have explored the role of the sphingolipid ceramide in exacerbating heart function with smoke exposure. Ceramide production is a consequence of cigarette smoke in the lung, and considering ceramide's harmful effects on mitochondrial function, we sought to elucidate the role of ceramide in mediating smoke-induced altered heart mitochondrial respiration. Lung cells were exposed to cigarette smoke extract and heart cells were exposed to the lung-cell conditioned medium. Adult male mice were exposed sidestream cigarette smoke for 8 weeks with dietary intervention and ceramide inhibition. Ceramides and heart cell or myocardial mitochondrial respiration were determined. Lung cell cultures revealed a robust response to cigarette smoke extract in both production and secretion of ceramides. Heart cells incubated with lung-cell conditioned medium revealed a pronounced inhibition of myocardial mitochondrial respiration, though this effect was mitigated with ceramide inhibition via myriocin. In vivo, heart ceramides increased roughly 600% in adult mice with long-term sidestream cigarette smoke exposure. This resulted in a significant ceramide-dependent reduction in left myocardial mitochondrial respiration, as heart mitochondria from the mice exposed to both smoke and myriocin injections respired normally. These results suggest ceramide to be an important mediator of altered myocardial mitochondrial function with cigarette smoke exposure. Thus, anti-ceramide therapies might be considered in the future to protect heart mitochondrial function with smoke exposure.
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Ojha, Krishna Raj. "Determination of Membrane Fluidity And Correlate Its Effect in Bulk Bacterial Cell Respiration." University of Akron / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=akron1589628392050675.

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Gilkerson, Robert W. "The cristal membrane adapts mitochondrial structure to respiratory function /." view abstract or download file of text, 2002. http://wwwlib.umi.com/cr/uoregon/fullcit?p3072583.

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Thesis (Ph. D.)--University of Oregon, 2002.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 102-119). Also available for download via the World Wide Web; free to University of Oregon users.
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Missarova, Alsu 1990. "mtDNA dynamics are a driving force of cell-to-cell heterogeneity in Saccharomyces cerevisiae." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/663194.

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Isogenic cells exhibit a large degree of cell-to-cell heterogeneity in proliferation, with a subpopulation of cells growing at a substantially lower rate. We conducted a high throughput microscopy screen to determine the proliferation distributions for a collection of wild isolates and 1592 single gene deletions in S. cerevisiae. We found that mitochondrial impairment is a primary cause of slow growth within an isogenic population and that high mitochondrial membrane potential is predictive of reduced growth and respiratory deficiency. We showed that respiratory deficiency can be recovered and that temporary respiratory deficiency is a common trait present in many genetic backgrounds. We developed a mathematical model that predicts the dynamics of the respiratory capacity of single cells within a population as a function of mtDNA state. Finally, we showed that growth in the antifungal agent fluconazole enriches for temporarily respiratory deficient cells, suggesting that this phenotype may be a form of bet-hedging in which a slow growing drug-resistant respiratory deficient cell with low mtDNA content can produce progeny with fast growth and fully functioning mitochondria.
Les cèl·lules isogèniques mostren un gran grau d' heterogenietat cel·lular en la seva taxa de proliferació, amb una subpoblació de cèl·lules creixent de manera substancialment lenta. Hem realitzat un assaig de microsopia d’alt rendiment (high-throughput) i hem determinat les distribucions de proliferació d'un conjunt de més de 1590 delecions de gens individuals i de soques wild type de Saccharomyces cerevisiae. Hem trobat que la disfunció mitocondrial és una causa primària del creixement lent dins d'una població isogènica i hem observat que un potencial alt de la membrana mitocondrial ens permet predir la reducció del creixement i la deficiència respiratòria. Hem mostrat que aquesta reducció es pot revertir en determinades circumstàncies i que la deficiència respiratòria temporal és un tret comú en moltes soques. També hem relacionat la dinàmica de la capacitat respiratòria d'una cèl·lula amb l’estat del seu ADN mitocondrial. Finalment, hem mostrat que el creixement en presència d'agents antifúngics augmenta el nombre de cèl·lules amb deficiència temporal respiratòria, suggerint que aquest fenotip pot ser una forma de protecció (subpoblació resistent als fàrmacs amb ADN mitocondrial intacte).
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Hart, A. J. "Physiology of growth and respiration during the cell cycles of Bacillus subtilis and Paracoccus denitrificans." Thesis, University of Liverpool, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356282.

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Liimatta, E. (Erkki). "Intracellular calcium, preconditioning and regulation of cellular respiration in heart." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514260865.

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Abstract Heart muscle has to work constantly throughout the life and its energy metabolism is heavily dependent on a continuous supply of oxygen. Energy metabolism must be effectively regulated to meet the demands of changing workloads in different circumstances. If the oxygen supply is interrupted, the function of the heart is easily disturbed and cells injured. Calcium metabolism is of great importance in these pathological conditions. In this thesis respiratory regulation was studied by non-destructive optical methods in mouse heart. The myoglobin-deficient mouse was used as an experimental model to avoid the artefact caused by intracellular myoglobin. Results show that increased consumption of energy and oxygen lead to concomitant reduction of cytochrome aa3 and oxidation of flavoproteins. This finding supports the view that cell respiration in intact myocardium is dominantly regulated at the level of the respiratory chain. The intracellular Ca2+ accumulation during ischemia is one of the major causes of irreversible ischemia-reperfusion injury. Ischemic preconditioning (IPC) has been shown to protect the heart muscle significantly from ischemic damage. In this thesis Ca2+ accumulation during ischemia and reperfusion was studied in perfused rat heart using Fura-2 as a fluorescent Ca2+ indicator. As there is a significant decrease in intracellular pH during prolonged ischemia, the pH-dependency of Fura-2 signal was taken into account. It was found that IPC attenuates Ca2+accumulation during ischemia and this was connected to a decrease in mitochondrial membrane potential. Both IPC and the pharmacologically induced preconditioning with the mitoKATP opener diaxozide were shown to be associated with increased production of superoxide monitored by means of lucigenin chemiluminescence. The superoxide production correlated with the oxidation-reduction state of flavoproteins. We also describe here a method for measuring of intracellular free Ca2+ in mouse heart during ischemia by simultaneous monitoring of Fura-2 and the pH probe BCECF fluorescence by means of dual wavelength excitation of both probes. The paradoxical decrease of Fura-2 fluorescence during ischemia indicating decreasing intracellular Ca2+ concentration was due to the pH effect on the dissociation constant of the Fura-2-Ca2+ complex. When the pH-dependency of Fura-2 was compensated, an extensive Ca2+ accumulation during ischemia was detected. Much of the previous literature on this subject must be re-evaluated because the pH-dependency of intracellular Ca2+ probes has been largely overlooked.
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Rowley, Thomas John. "The Effect of Cocoa Flavanols on β-Cell Mass and Function." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6508.

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A hallmark of type 2 diabetes (T2D) is β-cell dysfunction and the eventual loss of functional β-cell mass. Therefore, mechanisms that improve or preserve β-cell function could be used to improve the quality of life of individuals with T2D. Studies have shown that monomeric, oligomeric and polymeric cocoa flavanols have different effects on obesity, insulin resistance and glucose tolerance. We hypothesized that these cocoa flavanols may have beneficial effects on β-cell function. INS-1 832/13 derived β-cells and primary rat islets cultured with a monomeric catechin-rich cocoa flavanol fraction demonstrated enhanced glucose-stimulated insulin secretion, while cells cultured with total cocoa extract, oligomeric, or polymeric procyanidin-rich fractions demonstrated no improvement. The increased glucose-stimulated insulin secretion in the presence of the monomeric catechin-rich fraction corresponded with enhanced mitochondrial respiration, suggesting improvements in β-cell fuel utilization. Mitochondrial complex III, IV and V components were upregulated after culture with the monomer-rich fraction, corresponding with increased cellular ATP production. The monomer-rich fraction improved cellular redox state and increased glutathione concentration, which corresponds with Nrf2 nuclear localization and expression of Nrf2 target genes, including NRF-1 and GABPA, essential genes for increasing mitochondrial function. We propose a model by which monomeric cocoa catechins improve the cellular redox state, resulting in Nrf2 nuclear migration and upregulation of genes critical for mitochondrial respiration, and, ultimately, enhanced glucose-stimulated insulin secretion and β-cell function. These results suggest a mechanism by which monomeric cocoa catechins exert their effects as an effective complementary strategy to benefit T2D patients.
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Aebig, Trudy J. "Cell cycle-dependent association of plectin 1b regulates mitochondrial morphology and function." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307440587.

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Books on the topic "Cell respiration"

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Roland, Douce, Day, D. A. 1949 July 27-, and Ap Rees T. 1930-, eds. Higher plant cell respiration. Berlin: Springer-Verlag, 1985.

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Douce, Roland, and David A. Day, eds. Higher Plant Cell Respiration. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6.

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Gijsbert, Osterhoudt, and Barhydt Jos, eds. Cell respiration and cell survival: Processes, types and effects. Hauppauge, N.Y: Nova Science Publishers, 2009.

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P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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Kramer, Stephen P. Getting oxygen: What do you do if you're cell twenty-two? New York: Crowell, 1986.

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O'Regan, R. G. Arterial chemoreceptors: Cell to system. New York: Springer Science+Business Media, LLC, 1994.

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The oxygen breakthrough: 30 days to an illness-free life. New York: Morrow, 1989.

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Han, Asard, Bérczi Alajos, and Caubergs Roland J, eds. Plasma membrane redox systems and their role in biological stress and disease. Dordrecht: Kluwer, 1998.

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J, López-Barneo, and Weir E. Kenneth, eds. Oxygen regulation of ion channels and gene expression. Armonk, N.Y: Futura Pub., 1998.

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Cancer: Between glycolysis and physical constraint. Berlin: Springer, 2004.

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Book chapters on the topic "Cell respiration"

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Day, D. A., and R. Douce. "Introduction." In Higher Plant Cell Respiration, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_1.

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Hanson, J. B. "Membrane Transport Systems of Plant Mitochondria." In Higher Plant Cell Respiration, 248–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_10.

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Wiskich, J. T., and I. B. Dry. "The Tricarboxylic Acid Cycle in Plant Mitochondria: Its Operation and Regulation." In Higher Plant Cell Respiration, 281–313. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_11.

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Gardeström, P., and G. E. Edwards. "Leaf Mitochondria (C3 + C4 + CAM)." In Higher Plant Cell Respiration, 314–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_12.

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Stitt, M., and M. Steup. "Starch and Sucrose Degradation." In Higher Plant Cell Respiration, 347–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_13.

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ap Rees, T. "The Organization of Glycolysis and the Oxidative Pentose Phosphate Pathway in Plants." In Higher Plant Cell Respiration, 391–417. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_14.

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Lambers, H. "Respiration in Intact Plants and Tissues: Its Regulation and Dependence on Environmental Factors, Metabolism and Invaded Organisms." In Higher Plant Cell Respiration, 418–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_15.

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Neuburger, M. "Preparation of Plant Mitochondria, Criteria for Assessement of Mitochondrial Integrity and Purity, Survival in Vitro." In Higher Plant Cell Respiration, 7–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_2.

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Quetier, F., B. Lejeune, S. Delorme, and D. Falconet. "Molecular Organization and Expression of the Mitochondrial Genome of Higher Plants." In Higher Plant Cell Respiration, 25–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_3.

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Harwood, J. L. "Plant Mitochondrial Lipids: Structure, Function and Biosynthesis." In Higher Plant Cell Respiration, 37–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70101-6_4.

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Conference papers on the topic "Cell respiration"

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Hu, Jianing. "Cell Respiration—Energy Production of Cells." In 2021 International Conference on Culture, Design and Social Development (CDSD 2021). Paris, France: Atlantis Press, 2022. http://dx.doi.org/10.2991/assehr.k.220109.016.

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Suzuki, Masayasu, Hiroyuki Tanaka, and Yasunori Iribe. "Detection and collection system of target single cell based on respiration and metabolic activity." In 2009 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2009. http://dx.doi.org/10.1109/mhs.2009.5351919.

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Hammoudi, Naima, Feng Wang, and Peng Huang. "Abstract 3314: Potential role of mitochondrial respiration in serum-induced tumor stem cell differentiation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3314.

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Rivadeneira, Dayana B., M. Cecilia Caino, Jae Ho Seo, Alessia Angelin, Wallace C. Douglas, Lucia R. Languino, and Dario C. Altieri. "Abstract B09: Mitochondrial respiration controlled by survivin directs mitochondrial dynamics and tumor cell invasion." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-b09.

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Pajic, Tanja, Miroslav Zivic, Mihailo Rabasovic, Aleksandar Krmpot, and Natasa Todorovic. "THE DAMPENING OF LIPID DROPLET OSCILLATORY MOVEMENT IN NITROGEN STARVED FILAMENTOUS FUNGI BY A LOW DOSE OF MITOCHONDRIAL RESPIRATION INHIBITOR." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.226p.

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Lipid droplets (LDs) are small mobile organelles conserved in all eukaryotic cells. We wanted to test if the LD movement can be muffled by an incomplete inhibition of mitochondrial respiration, induced by treating hyphae of filamentous fungus Phycomyces blakesleeanus with 0.5 mM sodium azide. Nitrogen starved hyphae were used, in order to obtain LDs in larger sizes and numbers. The data obtained unequivocally showed: 1. Sodium azide treatment dramatically reduces the LD velocity and the distances LDs travel; 2. LDs in both controls and in azide-treated hyphae oscillate in a small confined space instead of travelling through the cell; 3. Azide-treated LDs oscillate less frequently and in smaller confinement than controls.
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Bubb, K., T. Holzer, J. L. Nolte, M. Krüger, R. Wilson, U. Schlötzer-Schrehardt, J. Brinckmann, et al. "Single cell RNA sequencing identifies mitochondrial respiration as a key factor contributing to extracellular matrix integrity." In III. MuSkITYR Symposium. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736714.

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Becker, Winston R., Matthew R. Webster, and Raffaella De Vita. "Variability in Mechanical Properties of Insect Tracheal Tubes." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14803.

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Insects employ a network of tracheal tubes to transport oxygen directly to every cell of the body. During respiration, these tubes undergo localized and rhythmic deformations due to local variation in their structural and mechanical properties. In order to elucidate the mechanisms of insect respiration, mechanical tests on ring sections of tracheal tubes extracted from American Cockroaches were conducted. A total of 33 specimens collected from 14 tracheal tubes located in the upper thorax of the insects were successfully tested. The ultimate tensile strength (22.6 ± 13.3 MPa), ultimate strain (1.57 ± 0.68 %), elastic modulus (1740 ± 840 MPa), and toughness (0.175 ± 0.156 MJm −3) were measured in the radial direction. The mechanical properties of ring sections excised from the same tracheal tube were shown to exhibit less variability than those of ring sections excised from different tracheal tubes. The results of this study will help in determining the relationship between the mechanics and structure of tracheal tube thus ultimately leading to the creation of novel bio-inspired micro-systems.
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Sainz, Bruno, Sonia Alcala Sanchez, and Mireia Vallespinos. "Abstract 1724: Pancreatic cancer stem cell metastasis and mitochondrial respiration is dependent on the the ISG15-mediated ubiquitin-like modification process known as ISGylation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1724.

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Kumar, A., J. Fareed, W. H. Wehrmacher, D. Hoppensteadt, O. Ulutin, and J. M. Walenga. "ENDOTHELIAL FUNCTION MODULATION AND CONTROL OF VASCULAR AND THROMBOTIC DISORDERS: EXPERIMENTAL RESULTS WITH A POLYDEOXY RIBONUCLEOTIDE AGENT DEFIBROTIDE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643149.

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Numerous approaches with single and multiple drugs modulating protease cascade, platelet function and blood viscosity and to reduce blood lipids to manage thrombotic processes have been tried. Defibrotide, a polydeoxyribonucleotide, (Mr =17,000) offers a new approach to vascular and related thrombotic processes as it acts via modulation of endothelial cell function. We have used a primate model (Macaca mulatta) to study the endogenous action of this agent after the oral (10-25 mg/kg) and intravenous (5-10 mg/kg) administration. This agent produced no effect on clotting tests and ex vivo laboratory findings but rather it elevated the t-PA (antigen and functional), protein C (antigen and functional), prostacyclin and decreased thromboxane, 01.2-antiplasmin (functional) and t-PA inhibitor (functional) in both studies. These observations suggest that Defibrotide modulates endothelial function. Hepatic isolation in rabbits totally blocked the antithrombotic actions of Defibrotide suggesting that this agent is converted into an active product endogenously. Pretreatment of Defibrotide with nucleases also resulted in a complete loss of its actions. Defibrotide produced dose dependent antithrombotic actions in animal models (rabbit venous stasis and rat vena caval ligation) after either intravenous or oral administration. Blood pressure, heart rate, respiration and kidney function were not altered by it. No effect on bleeding time was noted in any studies. Upon oral administration this drug produced pharmacologic action after 2 hours whereas after intravenous administration, the action peaked at 30 minutes. Defibrotide exhibited cytoprotective effects towards endothelial lining of the vascular smooth muscles characterized by microscopic studies. In summary Defibrotide is an endothelial support agent whose multicomponent actions are primarily mediated via the physical and functional modulation of the endothelial cells in the vascular system.
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Merrikh, A. A., and J. L. Lage. "Effect of Moving Capillary Red Blood Cells on Alveolar Respiration." In ASME 2003 Heat Transfer Summer Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/ht2003-47558.

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Researchers in the open literature have focused on developing methods to estimate the lung diffusing capacity (DL) both theoretically and experimentally because of the continuous interest in understanding the gas transfer phenomenon of respiration.
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Reports on the topic "Cell respiration"

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Raich, J. W. Interannual Variability in Global Soil Respiration on a 0.5 Degree Grid Cell Basis (1980-1994). Office of Scientific and Technical Information (OSTI), September 2003. http://dx.doi.org/10.2172/885610.

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Delmer, Deborah P., and Prem S. Chourey. The Importance of the Enzyme Sucrose Synthase for Cell Wall Synthesis in Plants. United States Department of Agriculture, October 1994. http://dx.doi.org/10.32747/1994.7568771.bard.

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The goal of this work was to understand the role of the enzyme sucrose synthase (SuSy) in synthesis of cellulose and callose in plants. The work resulting from the this grant leads to a number of conclusions. SuSy clearly plays diverse roles in carbon metabolism. It can associate with the plasma membrane of cells undergoing rapid cellulose deposition, such as cotton fibers, developing maize endosperm, gravistimulated pulvini, and transfer cells of the cotton seed. It is also concentrated at sites of high callose deposition (tapetal cells; cell plates). When SuSy levels are lowered by mutation or by anti-sense technology, cell walls undergo degeneration (maize endosperm) and show reduced levels of cellulose (potato tubers). In sum, our evidence has very much strengthened the concept that SuSy does function in the plasma membrane to channel carbon from sucrose via UDP-glucose to glucan synthase complexes. Soluble SuSy also clearly plays a role in providing carbon for starch synthesis and respiration. Surprisingly, we found that the cotton seed is one unique case where SuSy apparently does not play a role in starch synthesis. Current evidence in sum suggests that no specific SuSy gene encodes the membrane-associated form, although in maize the SS 1 form of SuSy may be most important for cell wall synthesis in the early stages of endosperm development. Work is still in progress to determine what does control membrane localization - and the current evidence we have favors a role for Ca2+, and possibly also protein phosphorylation by differentially regulated protein kinases. Finally, we have discovered for the first time, a major new family of genes that encode the catalytic subunit of the cellulose synthase of plants - a result that has been widely cited and opens many new approaches for the study of this important plant function.
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Pesis, Edna, and Mikal Saltveit. Postharvest Delay of Fruit Ripening by Metabolites of Anaerobic Respiration: Acetaldehyde and Ethanol. United States Department of Agriculture, October 1995. http://dx.doi.org/10.32747/1995.7604923.bard.

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The use of pretreatments for 24 h prior to storage, under anaerobic condtions, or in the presence of the natural metabolic products, acetaldehyde (AA) and ethanol, to delay fruit ripening, was found to be effective with several climacteric fruits, among them avocado, mango, peach and tomato. The delay in ripening of avocado, peach and tomato was accompanied by inhibition of ethylene production and of fruit softening. The maintenance of fruit firmness was associated with a decrease in the activities of cell-wall-degrading enzymes, including endoglucanases (Cx), polygalacturonases (PG) and b-galactosidases. In peaches the AA- and N2-treated fruits were firmer after 3 weeks storage and contained higher amount of insoluble pectin than untreated controls. We showed that AA vapors are able to inhibit ripening, ethylene production and ethylene induction in the presence of 1-amino-cyclopropane-1-carboxylic acid (ADD) in avocado and mango tissue. Ethylene induced by ACC is taken as an indicator of ACC oxidase activity. ACC oxidase activity in AA-treated avocado fruit was much lower than in the untreated fruit. In carnation flowers very little ethylene was produced by ethanol-treated flowers, and the normal increases in ACC content and ACC oxidase activity were also suppressed. Using kinetic studies and inhibitors of alcohol dehydrogenase (ADH), we showed that AA, not ethanol, was the active molecule in inhibiting ripening of tomato fruit. Application of anaerobiosis or anaerobic metabolites was effective in reduction of chilling injury (CI) in various plant tissues. Pretreatment with a low-O2 atmosphere reduced CI symptoms in avocado; this effect was associated with higher content of the free sylfhydryl (SH) group, and induction of the detoxification enzymes, catalase and peroxidase. Application of AA maintained firmer and brighter pulp tissue (non-oxidative), which was associated with higher free SH content, lower ethylene and ACC oxidase activities, and higher activities of catalase and peroxidase. Ethanol was found to reduce CI in other plant tissue. In roots of 24-h-old germinated cucumber seeds, exposure to 0.4-M ethanol shock for 4 h reduced chilling-induced ion leakage. In cucumber cotyledons it appears that alcohols may reduce CI by inducing stomata closure. In cotyledon discs held in N2 at 10C for 1 day, there accumulated sufficient endogenously synthesized ethanol to confer tolerance to chilling at 2.5C for 5 days.
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Porat, Ron, Gregory T. McCollum, Amnon Lers, and Charles L. Guy. Identification and characterization of genes involved in the acquisition of chilling tolerance in citrus fruit. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7587727.bard.

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Citrus, like many other tropical and subtropical fruit are sensitive to chilling temperatures. However, application of a pre-storage temperature conditioning (CD) treatment at 16°C for 7 d or of a hot water brushing (HWB) treatment at 60°C for 20 sec remarkably enhances chilling tolerance and reduces the development of chilling injuries (CI) upon storage at 5°C. In the current research, we proposed to identify and characterize grapefruit genes that are induced by CD, and may contribute to the acquisition of fruit chilling tolerance, by two different molecular approaches: cDNA array analysis and PCR cDNA subtraction. In addition, following the recent development and commercialization of the new Affymetrix Citrus Genome Array, we further performed genome-wide transcript profiling analysis following exposure to CD and chilling treatments. To conduct the cDNA array analysis, we constructed cDNA libraries from the peel tissue of CD- and HWB-treated grapefruit, and performed an EST sequencing project including sequencing of 3,456 cDNAs from each library. Based on the obtained sequence information, we chose 70 stress-responsive and chilling-related genes and spotted them on nylon membranes. Following hybridization the constructed cDNA arrays with RNA probes from control and CD-treated fruit and detailed confirmations by RT-PCR analysis, we found that six genes: lipid-transfer protein, metallothionein-like protein, catalase, GTP-binding protein, Lea5, and stress-responsive zinc finger protein, showed higher transcript levels in flavedo of conditioned than in non-conditioned fruit stored at 5 ᵒC. The transcript levels of another four genes: galactinol synthase, ACC oxidase, temperature-induced lipocalin, and chilling-inducible oxygenase, increased only in control untreated fruit but not in chilling-tolerant CD-treated fruit. By PCR cDNA subtraction analysis we identified 17 new chilling-responsive and HWB- and CD-induced genes. Overall, characterization of the expression patterns of these genes as well as of 11 more stress-related genes by RNA gel blot hybridizations revealed that the HWB treatment activated mainly the expression of stress-related genes(HSP19-I, HSP19-II, dehydrin, universal stress protein, EIN2, 1,3;4-β-D-glucanase, and SOD), whereas the CD treatment activated mainly the expression of lipid modification enzymes, including fatty acid disaturase2 (FAD2) and lipid transfer protein (LTP). Genome wide transcriptional profiling analysis using the newly developed Affymetrix Citrus GeneChip® microarray (including 30,171 citrus probe sets) revealed the identification of three different chilling-related regulons: 1,345 probe sets were significantly affected by chilling in both control and CD-treated fruits (chilling-response regulon), 509 probe sets were unique to the CD-treated fruits (chilling tolerance regulon), and 417 probe sets were unique to the chilling-sensitive control fruits (chilling stress regulon). Overall, exposure to chilling led to expression governed arrest of general cellular metabolic activity, including concretive down-regulation of cell wall, pathogen defense, photosynthesis, respiration, and protein, nucleic acid and secondary metabolism. On the other hand, chilling enhanced various adaptation processes, such as changes in the expression levels of transcripts related to membranes, lipid, sterol and carbohydrate metabolism, stress stimuli, hormone biosynthesis, and modifications in DNA binding and transcription factors.
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Hochman, Ayala, Thomas Nash III, and Pamela Padgett. Physiological and Biochemical Characterization of the Effects of Oxidant Air Pollutants, Ozone and Gas-phase Nitric Acid, on Plants and Lichens for their Use as Early Warning Biomonitors of these Air Pollutants. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697115.bard.

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Introduction. Ozone and related oxidants are regarded as the most important phytotoxic air pollutant in many parts of the western world. A previously unrecognized component of smog, nitric acid, may have even greater deleterious effects on plants either by itself or by augmenting ozone injury. The effects of ozone on plants are well characterized with respect to structural and physiological changes, but very little is known about the biochemical changes in plants and lichens exposed to ozone and/or HNO3. Objectives.To compare and contrast the responses of crop plants and lichens to dry deposition of HNO3 and O3., separately, and combined in order to assess our working hypothesis that lichens respond to air pollution faster than plants. Lichens are most suitable for use as biomonitors because they offer a live-organism-based system that does not require maintenance and can be attached to any site, without the need for man-made technical support systems. Original Immediate aims To expose the tobacco (Nicotiana tabacum L.) cultivar Bel-W3 that is ozone supersensitive and the ozone sensitive red kidney bean (Phaseolusvulgaris) and the lichen Ramalinamenziesii to controlled HNO3 and O3 fumigations and combined and to follow the resulting structural, physiological and biochemical changes, with special reference to reactive oxygen species related parameters. Revised. Due to technical problems and time limitations we studied the lichen Ramalinamenziesii and two cultivar of tobacco: Bel-W3 that is ozone supersensitive and a resistant cultivar, which were exposed to HNO3 and O3 alone (not combined). Methodology. Plants and lichens were exposed in fumigation experiments to HNO3 and O3, in constantly stirred tank reactors and the resulting structural, physiological and biochemical changes were analyzed. Results. Lichens. Exposure of Ramalinamenziesiito HNO3 resulted in cell membrane damage that was evident by 14 days and continues to worsen by 28 days. Chlorophyll, photosynthesis and respiration all declined significantly in HNO3 treatments, with the toxic effects increasing with dosage. In contrast, O3 fumigations of R. menziesii showed no significant negative effects with no differences in the above response variables between high, moderate and low levels of fumigations. There was a gradual decrease in catalase activity with increased levels of HNO3. The activity of glutathione reductase dropped to 20% in thalli exposed to low HNO3 but increased with its increase. Glucose 6-phosphate dehydrogenase activity increase by 20% with low levels of the pollutants but decreased with its increase. Tobacco. After 3 weeks of exposure of the sensitive tobacco cultivar to ozone there were visible symptoms of toxicity, but no danmage was evident in the tolerant cultivar. Neither cultivar showed any visible symptoms after exposure to HNO3.In tobacco fumigated with O3, there was a significant decrease in maximum photosynthetic CO2 assimilation and stomatal conductance at high levels of the pollutant, while changes in mesophyll conductance were not significant. However, under HNO3 fumigation there was a significant increase in mesophyll conductance at low and high HNO3 levels while changes in maximum photosynthetic CO2 assimilation and stomatal conductance were not significant. We could not detect any activity of the antioxidant enzymes in the fumigated tobacco leaves. This is in spite of the fact that we were able to assay the enzymes in tobacco leaves grown in Israel. Conclusions. This project generated novel data, and potentially applicable to agriculture, on the differential response of lichens and tobacco to HNO3 and O3 pollutants. However, due to experimental problems and time limitation discussed in the body of the report, our data do not justify yet application for a full, 4-year grant. We hope that in the future we shall conduct more experiments related to our objectives, which will serve as a basis for a larger scale project to explore the possibility of using lichens and/or plants for biomonitoring of ozone and nitric acid air pollution.
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Izhar, Shamay, Maureen Hanson, and Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7604933.bard.

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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.
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Banin, Amos, Joseph Stucki, and Joel Kostka. Redox Processes in Soils Irrigated with Reclaimed Sewage Effluents: Field Cycles and Basic Mechanism. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7695870.bard.

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The overall objectives of the project were: (a) To measure and study in situ the effect of irrigation with reclaimed sewage effluents on redox processes and related chemical dynamics in soil profiles of agricultural fields. (b) To study under controlled conditions the kinetics and equilibrium states of selected processes that affect redox conditions in field soils or that are effected by them. Specifically, these include the effects on heavy metals sorption and desorption, and the effect on pesticide degradation. On the basis of the initial results from the field study, increased effort was devoted to clarifying and quantifying the effects of plants and water regime on the soil's redox potential while the study of heavy metals sorption was limited. The use of reclaimed sewage effluents as agricultural irrigation water is increasing at a significant rate. The relatively high levels of suspended and, especially, dissolved organic matter and nitrogen in effluents may affect the redox regime in field soils irrigated with them. In turn, the changes in redox regime may affect, among other parameters, the organic matter and nitrogen dynamics of the root zone and trace organic decomposition processes. Detailed data of the redox potential regime in field plots is lacking, and the detailed mechanisms of its control are obscure and not quantified. The study established the feasibility of long-term, non-disturbing monitoring of redox potential regime in field soils. This may enable to manage soil redox under conditions of continued inputs of wastewater. The importance of controlling the degree of wastewater treatment, particularly of adding ultrafiltration steps and/or tertiary treatment, may be assessed based on these and similar results. Low redox potential was measured in a field site (Site A, KibutzGivat Brenner), that has been irrigated with effluents for 30 years and was used for 15 years for continuous commercial sod production. A permanently reduced horizon (Time weighted averaged pe= 0.33±3.0) was found in this site at the 15 cm depth throughout the measurement period of 10 months. A drastic cultivation intervention, involving prolonged drying and deep plowing operations may be required to reclaim such soils. Site B, characterized by a loamy texture, irrigated with tap water for about 20 years was oxidized (Time weighted average pe=8.1±1.0) throughout the measurement period. Iron in the solid phases of the Givat Brenner soils is chemically-reduced by irrigation. Reduced Fe in these soils causes a change in reactivity toward the pesticide oxamyl, which has been determined to be both cytotoxic and genotoxic to mammalian cells. Reaction of oxamyl with reduced-Fe clay minerals dramatically decreases its cytotoxicity and genotoxicity to mammalian cells. Some other pesticides are affected in the same manner, whereas others are affected in the opposite direction (become more cyto- and genotoxic). Iron-reducing bacteria (FeRB) are abundant in the Givat Brenner soils. FeRB are capable of coupling the oxidation of small molecular weight carbon compounds (fermentation products) to the respiration of iron under anoxic conditions, such as those that occur under flooded soil conditions. FeRB from these soils utilize a variety of Fe forms, including Fe-containing clay minerals, as the sole electron acceptor. Daily cycles of the soil redox potential were discovered and documented in controlled-conditions lysimeter experiments. In the oxic range (pe=12-8) soil redox potential cycling is attributed to the effect of the daily temperature cycle on the equilibrium constant of the oxygenation reaction of H⁺ to form H₂O, and is observed under both effluent and freshwater irrigation. The presence of plants affects considerably the redox potential regime of soils. Redox potential cycling coupled to the irrigation cycles is observed when the soil becomes anoxic and the redox potential is controlled by the Fe(III)/Fe(II) redox couple. This is particularly seen when plants are grown. Re-oxidation of the soil after soil drying at the end of an irrigation cycle is affected to some degree by the water quality. Surprisingly, the results suggest that under certain conditions recovery is less pronounced in the freshwater irrigated soils.
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