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Artykuły w czasopismach na temat "Physiological oxidation"

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Tardo-Dino, Pierre-Emmanuel, Julianne Touron, Stéphane Baugé, Stéphanie Bourdon, Nathalie Koulmann i Alexandra Malgoyre. "The effect of a physiological increase in temperature on mitochondrial fatty acid oxidation in rat myofibers". Journal of Applied Physiology 127, nr 2 (1.08.2019): 312–19. http://dx.doi.org/10.1152/japplphysiol.00652.2018.

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We investigated the effect of temperature increase on mitochondrial fatty acid (FA) and carbohydrate oxidation in the slow-oxidative skeletal muscles (soleus) of rats. We measured mitochondrial respiration at 35°C and 40°C with the physiological substrates pyruvate + 4 mM malate (Pyr) and palmitoyl-CoA (PCoA) + 0.5 mM malate + 2 mM carnitine in permeabilized myofibers under nonphosphorylating ([Formula: see text]) or phosphorylating ([Formula: see text]) conditions. Mitochondrial efficiency was calculated by the respiratory control ratio (RCR = [Formula: see text]/[Formula: see text]). We used guanosine triphosphate (GTP), an inhibitor of uncoupling protein (UCP), to study the mechanisms responsible for alterations of mitochondrial efficiency. We measured hydrogen peroxide (H2O2) production under nonphosphorylating and phosphorylating conditions at both temperatures and substrates. We studied citrate synthase (CS) and 3-hydroxyl acyl coenzyme A dehydrogenase (3-HAD) activities at both temperatures. Elevating the temperature from 35°C to 40°C increased PCoA-[Formula: see text] and decreased PCoA-RCR, corresponding to the uncoupling of oxidative phosphorylation (OXPHOS). GTP blocked the heat-induced increase of PCoA-[Formula: see text]. Rising temperature moved toward a Pyr-[Formula: see text] increase, without significance. Heat did not alter H2O2 production, resulting from either PCoA or Pyr oxidation. Heat induced an increase in 3-HAD but not in CS activities. In conclusion, heat induced OXPHOS uncoupling for PCoA oxidation, which was at least partially mediated by UCP and independent of oxidative stress. The classically described heat-induced glucose shift may actually be mostly due to a less efficient FA oxidation. These findings raise questions concerning the consequences of heat-induced alterations in mitochondrial efficiency of FA metabolism on thermoregulation. NEW & NOTEWORTHY Ex vivo exposure of skeletal myofibers to heat uncouples substrate oxidation from ADP phosphorylation, decreasing the efficiency of mitochondria to produce ATP. This heat effect alters fatty acids (FAs) more than carbohydrate oxidation. Alteration of FA oxidation involves uncoupling proteins without inducing oxidative stress. This alteration in lipid metabolism may underlie the preferential use of carbohydrates in the heat and could decrease aerobic endurance.
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Kelley, D. E., J. P. Reilly, T. Veneman i L. J. Mandarino. "Effects of insulin on skeletal muscle glucose storage, oxidation, and glycolysis in humans". American Journal of Physiology-Endocrinology and Metabolism 258, nr 6 (1.06.1990): E923—E929. http://dx.doi.org/10.1152/ajpendo.1990.258.6.e923.

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The effects of physiological hyperinsulinemia (approximately 75 mU/l) on glucose storage, oxidation, and glycolysis in skeletal muscle were assessed with euglycemic clamps performed in seven healthy volunteers, in conjunction with leg balance for glucose, lactate, alanine, O2, and CO2. Infusion of insulin increased leg glucose uptake, storage, and oxidation but did not alter net release of lactate and alanine. The respiratory quotient (RQ) across the leg increased from a basal value of 0.74 +/- 0.02 to 0.99 +/- 0.02 during hyperinsulinemia. Under conditions of insulin stimulation, 49 +/- 5% of leg glucose uptake was stored, 37 +/- 4% was oxidized, and 14 +/- 2% was released as lactate and alanine. We conclude that during physiological hyperinsulinemia and euglycemia 1) skeletal muscle lipid oxidation is nearly entirely suppressed and glucose becomes the primary oxidative substrate of muscle, 2) glucose storage and oxidation are the major pathways of skeletal muscle glucose metabolism and are quantitatively similar at physiological insulin levels, and 3) the majority of insulin-stimulated glycolysis is oxidized, with only a small portion released as lactate or alanine.
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Stadtman, E. R., i C. N. Oliver. "Metal-catalyzed oxidation of proteins. Physiological consequences". Journal of Biological Chemistry 266, nr 4 (luty 1991): 2005–8. http://dx.doi.org/10.1016/s0021-9258(18)52199-2.

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Thomas, Michael J. "Physiological aspects of low-density lipoprotein oxidation". Current Opinion in Lipidology 11, nr 3 (czerwiec 2000): 297–301. http://dx.doi.org/10.1097/00041433-200006000-00011.

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Drazic, Adrian, i Jeannette Winter. "The physiological role of reversible methionine oxidation". Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1844, nr 8 (sierpień 2014): 1367–82. http://dx.doi.org/10.1016/j.bbapap.2014.01.001.

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Ford, Megan M., Amanda L. Smythers, Evan W. McConnell, Sarah C. Lowery, Derrick R. J. Kolling i Leslie M. Hicks. "Inhibition of TOR in Chlamydomonas reinhardtii Leads to Rapid Cysteine Oxidation Reflecting Sustained Physiological Changes". Cells 8, nr 10 (28.09.2019): 1171. http://dx.doi.org/10.3390/cells8101171.

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The target of rapamycin (TOR) kinase is a master metabolic regulator with roles in nutritional sensing, protein translation, and autophagy. In Chlamydomonas reinhardtii, a unicellular green alga, TOR has been linked to the regulation of increased triacylglycerol (TAG) accumulation, suggesting that TOR or a downstream target(s) is responsible for the elusive “lipid switch” in control of increasing TAG accumulation under nutrient limitation. However, while TOR has been well characterized in mammalian systems, it is still poorly understood in photosynthetic systems, and little work has been done to show the role of oxidative signaling in TOR regulation. In this study, the TOR inhibitor AZD8055 was used to relate reversible thiol oxidation to the physiological changes seen under TOR inhibition, including increased TAG content. Using oxidized cysteine resin-assisted capture enrichment coupled with label-free quantitative proteomics, 401 proteins were determined to have significant changes in oxidation following TOR inhibition. These oxidative changes mirrored characterized physiological modifications, supporting the role of reversible thiol oxidation in TOR regulation of TAG production, protein translation, carbohydrate catabolism, and photosynthesis through the use of reversible thiol oxidation. The delineation of redox-controlled proteins under TOR inhibition provides a framework for further characterization of the TOR pathway in photosynthetic eukaryotes.
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Bonadonna, R. C., S. del Prato, E. Bonora, G. Gulli, A. Solini i R. A. DeFronzo. "Effects of physiological hyperinsulinemia on the intracellular metabolic partition of plasma glucose". American Journal of Physiology-Endocrinology and Metabolism 265, nr 6 (1.12.1993): E943—E953. http://dx.doi.org/10.1152/ajpendo.1993.265.6.e943.

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Methodology for assessing the glycolytic and oxidative fluxes from plasma glucose, by measuring 3H2O and 14CO2 rates of production during [3-3H]- and [U-14C]glucose infusion, was tested in healthy subjects. In study 1, during staircase 3H2O infusion in six subjects, calculated rates of 3H2O appearance agreed closely with 3H2O infusion rates. In study 2, when [2-3H]glucose and NaH14CO3 were infused in four subjects in the basal state and during a 4-h euglycemic insulin (approximately 70 microU/ml) clamp, accurate estimates of the rates of [2-3H]glucose detritiation were obtained (94-97% of the expected values), and the recovery factor of NaH14CO3 did not change during hyperinsulinemia. In study 3, 11 subjects underwent a 4-h euglycemic insulin (approximately 70 microU/ml) clamp with [3-3H]- and [U-14C]glucose infusion and measurement of gaseous exchanges by indirect calorimetry to estimate the rates of total glycolysis, glycogen synthesis, glucose oxidation, nonoxidative glycolysis, hepatic glucose production, glucose recycling, and glucose conversion to fat. Hyperinsulinemia stimulated glycogen synthesis above baseline more than glycolysis [increment of 4.78 +/- 0.37 vs. 2.0 +/- 0.17 mg.min-1 x kg-1 of lean body mass (LBM), respectively, P < 0.01] and incompletely suppressed (approximately 87%) hepatic glucose production. The major component of nonoxidative glycolysis shifted from glucose recycling in the postabsorptive state (approximately 57% of nonoxidative glycolysis) to glucose conversion to fat during hyperinsulinemia (approximately 59% of nonoxidative glycolysis). Lipid oxidation during the insulin clamp was negatively correlated with both isotopic glucose oxidation (r = -0.822, P < 0.002) and glycolysis (r = -0.582, P < 0.07). In conclusion, in healthy subjects, glycogen synthesis plays a greater role than glycolysis and glucose oxidation in determining insulin-mediated glucose disposal. Part of insulin-mediated increase in glycolysis/oxidation might be secondary to the relief of the competition between fat and glucose for oxidation.
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Hirota, Yuko, Dongchon Kang i Tomotake Kanki. "The Physiological Role of Mitophagy: New Insights into Phosphorylation Events". International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/354914.

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Mitochondria play an essential role in oxidative phosphorylation, fatty acid oxidation, and the regulation of apoptosis. However, this organelle also produces reactive oxygen species (ROS) that continually inflict oxidative damage on mitochondrial DNA, proteins, and lipids, which causes further production of ROS. To oppose this oxidative stress, mitochondria possess quality control systems that include antioxidant enzymes and the repair or degradation of damaged mitochondrial DNA and proteins. If the oxidative stress exceeds the capacity of the mitochondrial quality control system, it seems that autophagy degrades the damaged mitochondria to maintain cellular homeostasis. Indeed, recent evidence from yeast to mammals indicates that the autophagy-dependent degradation of mitochondria (mitophagy) contributes to eliminate dysfunctional, aged, or excess mitochondria. In this paper, we describe the molecular processes and regulatory mechanisms of mitophagy in yeast and mammalian cells.
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Harper, M. E., R. M. Dent, V. Bezaire, A. Antoniou, A. Gauthier, S. Monemdjou i R. McPherson. "UCP3 and its putative function: consistencies and controversies". Biochemical Society Transactions 29, nr 6 (1.11.2001): 768–73. http://dx.doi.org/10.1042/bst0290768.

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The physiological function of uncoupling protein 3 (UCP3) is as yet unknown. Based on its 57% homology to UCP1 whose physiologic function is uncoupling and thermogenesis, UCP3 was attributed with the function of mitochondrial uncoupling through proton-leak reactions. UCP3 is expressed selectively in muscle, a tissue in which it has been estimated that proton leak accounts for approx. 50% of resting energy metabolism. Genetic linkage, association and variant studies suggest a role for UCP3 in obesity and/or diabetes. Studies of the heterologous expression of UCP3 in yeast provide support for the idea that UCP3 can uncouple mitochondrial oxidative phosphorylation, but the physiological relevance of these results is questionable. In vitro studies of mitochondria from Ucp3− − mice provide support, but there are no changes in resting metabolic rate (RMR) of mice. In vivo studies demonstrate increased ATP synthesis, but estimates of substrate oxidation rate indicate no change. Mice that greatly overexpress Ucp3 in muscle have increased RMR. Inconsistent with the function of uncoupling are the observations that fasting results in increased expression of UCP3, but no change in muscle proton leak. Moreover, fasting decreases energy expenditure in muscle. Expression patterns for Ucp3 and lipid-metabolism genes support a physiological role in fatty acid oxidation. Overall, findings support a role for Ucp3 in fatty acid metabolism that may have implications for obesity and/or Type II diabetes.
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Burgoyne, Joseph R., i Philip Eaton. "Contemporary techniques for detecting and identifying proteins susceptible to reversible thiol oxidation". Biochemical Society Transactions 39, nr 5 (21.09.2011): 1260–67. http://dx.doi.org/10.1042/bst0391260.

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Elevated protein oxidation is a widely reported hallmark of most major diseases. Historically, this ‘oxidative stress’ has been considered causatively detrimental, as the protein oxidation events were interpreted simply as damage. However, recent advances have changed this antiquated view; sensitive methodology for detecting and identifying proteins susceptible to oxidation has revealed a fundamental role for this modification in physiological cell signalling during health. Reversible protein oxidation that is dynamically coupled with cellular reducing systems allows oxidative protein modifications to regulate protein function, analogous to phosphoregulation. However, the relatively labile nature of many reversible protein oxidation states hampers the reliable detection and identification of modified proteins. Consequently, specialized methods to stabilize protein oxidation in combination with techniques to detect specific types of modification have been developed. Here, these techniques are discussed, and their sensitivity, selectivity and ability to reliably identify reversibly oxidized proteins are critically assessed.
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Rozprawy doktorskie na temat "Physiological oxidation"

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O'Hagan, C. E. "Physiological catalysts of LDL oxidation". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396887.

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Bozac, Anna Elena. "Determining exogenous glucose oxidation during moderate exercise". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28736.

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The purpose of this study was to determine the quantity of a glucose drink oxidized during cycle ergometer exercise at 60% VO₂max for 75 minutes. A second purpose was to determine if the glucose drink improved sprint time to exhaustion at 90% VO₂max after 75 minutes of exercise. Six trained male cyclists (VO₂max > 60 ml•kg⁻¹•min•¹) exercised on three occasions during which they ingested either water ad lib (W), ¹³C-cornsyrup (100 g, 2.02 M) + water ad lib (CS), or NaH¹²CO₃/NaH¹³CO₃ mixture (5 mg•kg⁻¹, 1% ¹³C-enriched) + water ad lib (B). Treatments B and CS were ingested after 5 minutes of cycling at 60% VO₂max. During exercise, there was no difference between treatments in plasma lactate response, changes in plasma volume, sprint time to exhaustion, or in respiratory exchange ratio (RER), VO₂, or VCO₂. RER showed a significant decline (p< .01) from 5 minutes (1.00±0.05, X±SD) to 75 minutes (0.96±0.05), and VO₂ showed a significant positive shift (p< .01) from 3.15(±0.29) to 3.52(±0.45) l•min⁻¹. A transient rise in plasma glucose was observed with CS. Changes from rest in ¹³C/¹²C ratio (∂13C) showed a significant increase (p< .01) following CS. Peak glucose oxidation rate was 7.26 g•15 min⁻¹ which occurred after 75 minutes. Total dose of exogenous ¹³C-glucose recovered as ¹³CO₂ (above baseline) was 22%. These observations suggest that (1) during moderate exercise of 75 minutes duration, oxidation of exogenous glucose occurs within 15 minutes but contributes marginally to total carbohydrate utilization as RER continued to fall with or without CS, and (2) sprint time to exhaustion after 75 minutes of cycling is not improved with glucose ingestion.
Education, Faculty of
Curriculum and Pedagogy (EDCP), Department of
Graduate
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Chang, Hui. "Oxidative stress in the retina an experimental study in the rat /". Lund : Dept. of Ophthalmology, University Hospital, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39725792.html.

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Kerry, Nicole Louise. "The effect of natural dietary antioxidants on low density lipoprotein oxidation and atherosclerosis /". Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phk418.pdf.

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Rein, Neil Berthold. "Biological sulphide oxidation in heterotrophic environments". Thesis, Rhodes University, 2002. http://hdl.handle.net/10962/d1003978.

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Acid mine drainage is a major environmental pollution concern associated with the mining of sulphide-containing ore bodies. Both physicochemical and biological options have been investigated for the treatment of acid mine drainage with recent interest in biological processes targeting low-cost and passive treatment applications. All acid mine drainage biological treatment processes are based to some extent on the activity of sulphate reducing bacteria, and their ability to reduce sulphate to sulphide in the presence of a range of carbon and electron donor sources. A portion of the sulphide produced may be consumed in the precipitation of heavy metals present in the mine drainage. Residual sulphide must be removed, not only due to its toxicity, but especially to prevent its reoxidation to sulphate where salinity reduction is a target of the treatment process. The partial oxidation of sulphide to elemental sulphur is an option that has received considerable attention and both physicochemical and biological options have been investigated. Biological processes have substantial potential cost advantages and run at ambient temperatures and pressures. However, the oxidation of sulphide to elemental sulphur is poised over a narrow redox range and process control to maintain optimum conditions remains a serious problem. In addition little has been reported in the literature on process control of sulphide oxidation to elemental sulphur, in the heterotrophic conditions prevailing in the reaction environment following sulphate reduction. This study undertook an investigation of biological sulphide oxidation under heterotrophic conditions in order to establish the effect of organic compounds on biological sulphide oxidation, and to determine whether the presence of organics, and associated heterotrophic oxygen consumption, may be manipulated to maintain the defined redox conditions required for the production of elemental sulphur. Biological sulphide oxidation under heterotrophic conditions was investigated in a series of flask experiments. Based on these results three different reactor configurations, a Fixed-Film Trickle Filter Reactor, Submerged Fixed-Film Reactor and a Silicone Tubular Reactor were used to investigate sulphur production. The flask studies indicated that organics, and associated heterotrophic metabolism in the presence of excess oxygen in the sulphide oxidation reaction environment, did contribute to the poising of redox conditions and thereby enabling the production of elemental sulphur. While the Fixed-Film Trickle Filter Reactor was found to be redox unstable, probably due to excess oxygen ingress to the system, a reduced oxygen challenge in the Submerged Fixed-Film Reactor configuration was found to be more successful for production of elemental sulphur. However, due to the production of a predominantly filamentous sulphur producing microbial population, recovery of sulphur from the column was intermittent and unpredictable. Extended residence times for produced sulphur on the column increased the likelihood for its eventual oxidation to sulphate. The Silicone Tubular Reactor was found to support a vigorous sulphide oxidising biofilm and produced elemental sulphur effectively. Electron microscopic studies showed that this occurred as both biologically produced sulphur and, probably mainly, as crystalline sulphur in the ortho-rhomic form. Given the linear extension of the sulphur production reaction environment it is was possible to investigate the sequence of the reaction mechanism in grater detail than is possible in mixed systems. Based on these findings a model explaining sulphur production under heterotrophic conditions has been proposed and is presented. The commercial implications of the development have also been noted.
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Collins, Tracey Helen. "Investigation into the Effects of Oxidative Stress on Reproductive Development". The University of Waikato, 2007. http://hdl.handle.net/10289/2364.

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Nuclear transfer (NT), or cloning, which is the transfer of a donor nucleus to a recipient enucleated oocyte, has been successfully achieved to produce viable offspring in many species. The process is very inefficient, as reprogramming of the donor nucleus is required, and losses are high throughout development. Placentation abnormalities are a common feature amongst cloned animals. Incomplete nuclear reprogramming and erroneous epigenetic imprinting may contribute to aberrant protein transcription and DNA mutations, affecting mitochondrial metabolism and inducing cellular stress. In vitro produced embryos under high oxygen culture conditions may also suffer oxidative stress, with the resulting reactive oxygen species causing mitochondrial DNA mutations and cellular stress similar to clones. In this study, expression of oxidative stress protein markers (Hsp60, SOD2, Hsp70) in NT cotyledons were compared to artificial insemination (AI) at different time points of gestation (days 50, 100, and 150). As a continuum of the oxidative stress investigation in cloned cotyledons, in vitro produced embryos were cultured under 20% oxygen compared to the control 7% oxygen laboratory standard culture, with oxidative stress protein markers examined between the groups at blastocyst stage (day 7) and day 15. Embryo morphology was also observed to determine apparent physiological differences between the treatment and control embryos. No previous studies to date have investigated the developmental effects of oxidative stress in day 15 bovine embryos. The significant differences in oxidative stress proteins observed at several time points in the NT and AI groups were not repeatable, possibly due to sample freeze/thaw degradation. Morphological differences observed between embryos cultured in 20% oxygen and control groups were visually apparent, although not quantified. At day 15 manganese superoxide dismutase expression was significantly lower in the 20% group compared to control. The 20% oxygen group did not show higher heat shock protein 60 expression than control, however the same results have been observed in another study at blastocyst stage. The results of this study suggest that the effect of oxidative stress on embryonic development is evident yet inconclusive in bovine NT cotyledons, however does not appear apparent in day 15 embryos following culture in 20% oxygen.
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Chen, Yuan-Han. "The active site chemistry of factor inhibiting HIF-1, coordination, bonding, and reaction". Amherst, Mass. : University of Massachusetts Amherst, 2009. http://scholarworks.umass.edu/dissertations/AAI3372258/.

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Yi, Dong-Hui Chemistry Faculty of Science UNSW. "The Study of Biomarkers of Protein Oxidative Damage and Aging by Mass Spectrometry". Awarded by:University of New South Wales. School of Chemistry, 1999. http://handle.unsw.edu.au/1959.4/17636.

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The physiologically important free radicals, nitrogen monoxide and superoxide, can combine to form the reactive intermediate peroxynitrite. Peroxynitrite can react with proteins and their constituent amino acids, such as tyrosine, resulting in protein peroxidation, oxidation and nitration. The nitration of proteins, assessed by the analysis of 3-nitrotyrosine, is a proposed index of pathophysiological activity of peroxynitrite. The aim of the work was to investigate the reaction products between peroxynitrite and protein, develop an assay for 3-nitrotyrosine and measure its levels in biological samples. To study the amino acid products arising from the reaction of peroxynitrite and protein, both liquid chromatography (LC) and gas chromatography (GC) combined with mass spectrometry (MS) were adopted. Approaches to 3-nitrotyrosine assay development were first, to take advantage of the intrinsic sensitivity of electron capture negative ionization GC-MS. Secondly, to avoid possible artefactual problems associated with the derivatisation step in GC-MS, an assay for 3-nitrotyrosine based on combined LC-MS-MS was developed. When a selection of peptides was exposed to peroxynitrite under physiological conditions in vitro, the hydrolysis products showed that 3-nitrotyrosine was the major product. Detectable minor products were 3,5-dinitrotyrosine and DOPA. The GC-MS assay was found to be fraught with difficulty due to artefactual formation of 3-nitrotyrosine. In order to quantify and correct for artefact formation, this complication was approached by incorporating a second isotopomer. This method, however, was confounded by large errors that reduced the overall sensitivity. Either negative or zero levels of endogenous 3-nitrotyrosine were found in tested samples after correction for artefact formation. The LC-MS-MS assay was then used to analyse 3-nitrotyrosine levels in a range of biological samples, including human plasma from healthy volunteers, synovial fluid samples from arthritis patients and tissue extracts from a mouse model of amyotropic lateral sclerosis. In contrast to published data, 3-nitrotyrosine levels were found to be below the limit of detection (1 pg/????L, 10 pg o/c) for all samples - a result somewhat consistent with the negative GC-MS data. It is suggested that the high 3-nitrotyrosine levels previously reported in the literature might reflect artefactual generation of 3-nitrotyrosine and that other approaches to assessing pathophysiological nitration should be sought in future.
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Telles, Scott Gerard. "Change in zinc permeability of lipid bilayers as a function of fluidity and oxidation". Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1061869.

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The main goal in my project was find out if the rate of zinc crossing the bilayer was either due to the fluidity of vesicles or the level of oxidation of the vesicles.To measure the oxidation a simple procedure called the TBA Test was used to measure each PC tested. The fluidity measurement was a calculation using the temperature the vesicles went from gel to liquid crystalline phase and the experimental temperature.Measuring the rate at which zinc crossed the bilayer was done using spectral changes that occur as zinc binds with APIII, a metal chelator entrapped inside the vesicles. To measure these rates we used k', the rate constant at which zinc is crossing the bilayer at a certain concentration and k, the second order diffusion rate constant which is the slope of k' vs. [Zn].The rates at which zinc was crossing the bilayer for each PC was then compared to the fluidity and oxidation levels for each PC. There was no direct correlation between the rates and fluidity but there was a good linear correlation between the rates and oxidation.So it seemed as if oxidation was the main reason zinc was crossing the bilayer so we wanted to see if our measurements could be obtained by biological cells. The comparison showed that rates obtained by biological cells can only be matched by the vesicle models when there oxidation levels are found to be high.In conclusion we believe that the reason zinc is crossing the bilayer is due to oxidation that occurs to the vesicle and as oxidation increases so do the rates at which zinc crosses the bilayer.
Department of Chemistry
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Wright, Adam. "Investigations of singlet oxygen-mediated amino acid, peptide and protein oxidation". Thesis, The University of Sydney, 2002. https://hdl.handle.net/2123/27830.

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Książki na temat "Physiological oxidation"

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Oxidation: The cornerstone of carcinogenesis : oxidation and tobacco smoke carcinogenesis, a relationship between cause and effect. [Germany?]: Springer, 2008.

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Channa, Reddy C., Hamilton Gordon A, Madyastha K. M, National Science Foundation (U.S.) i Symposium on Biological Oxidation Systems (1989 : Bangalore, India), red. Biological oxidation systems. San Diego: Academic Press, 1990.

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J, Grabke H., i Schütze Michael, red. Oxidation of intermetallics. Weinheim: Wiley-VCH, 1998.

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Werner, Petra. Otto Warburgs Beitrag zur Atmungstheorie: Das Problem der Sauerstoffaktivierung. Marburg/Lahn: Basilisken-Presse, 1996.

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Mukhopadhyay, Satya N. Oxygen responses, reactivities, and measurements in biosystems. Boca Raton: CRC Press, 1994.

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M, Smeitink Jan A., Sengers Rob C. A i Trijbels J. M. Frans, red. Oxidative phosphorylation in health and disease. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2004.

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Oxidants in biology: A question of balance. [Siena, Italy?]: Springer, 2008.

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1931-, Armstrong Donald, red. Oxidants and antioxidants: Ultrastructure and molecular biology protocols. Totowa, N.J: Humana Press, 2002.

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Oxidative stress in aquatic ecosystems. Hoboken, NJ: Wiley-Blackwell, 2011.

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1934-, Hlavica P., i Damani L. A. 1949-, red. N-oxidation of drugs: Biochemistry, pharmacology, toxicology. London: Chapman & Hall, 1991.

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Części książek na temat "Physiological oxidation"

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Osmundsen, H., M. S. Thomassen, J. K. Hiltunen i R. K. Berge. "Physiological Role of Peroxisomal Beta-Oxidation". W Proceedings in Life Sciences, 152–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71325-5_14.

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Moreaux, V., I. Birlouez-Aragon, F. Tessier, H. Mondon, P. Junes i J. M. Lecerf. "Trp Oxidation by Copper-Ascorbate under Physiological Conditions". W Advances in Experimental Medicine and Biology, 719–26. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_115.

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Mildaziene, Vida, Rasa Baniene, Ausra Marcinkeviciute, Zita Nauciene, Alvydas Kalvenas i Aurelijus Zimkus. "Tetraphenylphosphonium inhibits oxidation of physiological substrates in heart mitochondria". W Detection of Mitochondrial Diseases, 67–70. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_10.

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Goodwin, Douglas C., Kimberley A. Laband i Kristen M. Hertwig. "Capsaicinoid Oxidation by Peroxidases: Kinetic, Structural, and Physiological Considerations". W ACS Symposium Series, 161–74. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0909.ch014.

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Wagner, Anneke M., Dirk-Jan Leek i Linus H. W. van der Plas. "NADPH Oxidation in Potato Tuber Callus Mitochondria and its Physiological Significance During in vivo Respiration". W Plant Mitochondria, 373–76. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3517-5_61.

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Larrigaudière, Christian, i Jordi Giné-Bordonaba. "Oxidative Stress and Physiological Disorders". W Postharvest Physiological Disorders in Fruits and Vegetables, 29–60. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2019. http://dx.doi.org/10.1201/b22001-3.

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du Plessis, Stefan S., Avi Harlev, Mohamed Iesar Mohamed, Eiad Habib, Narasimhan Kothandaraman i Zeynep Cakar. "Physiological Roles of Reactive Oxygen Species (ROS) in the Reproductive System". W Oxidative Stress in Human Reproduction, 47–64. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48427-3_3.

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Youdim, M. B. H., i Margarethe Holzbauert. "Physiological Aspects of the Oxidative Deamination of Monoamines". W Novartis Foundation Symposia, 105–33. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720219.ch7.

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Izzotti, Alberto. "The Physiological and Pathological Roles of Oxidative Damage to DNA in Relation to Life Stage". W Oxidative Damage to Nucleic Acids, 167–77. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9_13.

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Visioli, Rancesco, i M. Carmen Crespo. "Chapter 7. Oxidative Stress and Response in Physiological Systems". W Food Chemistry, Function and Analysis, 246–61. Cambridge: Royal Society of Chemistry, 2021. http://dx.doi.org/10.1039/9781839165337-00246.

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Streszczenia konferencji na temat "Physiological oxidation"

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De Paula, Iron Francisco. "Gene identification and physiological regulation of theB-oxidation pathway inRhodnius prolixus". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.112788.

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Benea, Lidia, Eliza Danaila, Valentin Marian Dumitrascu i Pierre Ponthiaux. "The effect of anodic oxidation treatment of Ti-10Zr alloy on tribocorrosion behavior in a simulated physiological solution". W 2015 E-Health and Bioengineering Conference (EHB). IEEE, 2015. http://dx.doi.org/10.1109/ehb.2015.7391574.

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Ibrahim, Hamdy. "A Micro Arc Oxidation Composite Coating Developed on a Biocompatible Magnesium Alloy for Bone Implant Applications". W ASME 2020 15th International Manufacturing Science and Engineering Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/msec2020-8492.

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Abstract The biocompatibility, mechanical properties and biodegradable nature of Mg alloys have made them attractive for biomedical applications, especially as bone implants. However, one of the main problems that limit the use of Mg alloy for several biomedical applications is their fast corrosion rates inside the body. Coating Mg-based implants is one of the most extensively studied approaches to address the fast corrosion rates of Mg alloys in the physiological environment. Micro arc oxidation (MAO) coating process has shown very promising results towards reducing the corrosion rates of Mg alloys due to the formation of a protective dense, well-adhered and wear-resistant oxide layer on the surface of the Mg alloy. In this study, the feasibility of coating an Mg-Zn-Ca-based alloy with a composite coating made using a micro-arc oxidation coating process and an immersion (dipping process) was investigated. The corrosion properties and surface characteristics of the coated alloy samples are assessed. The created protective composite coating is used to slow the corrosion rates of an Mg-Zn-Ca-based alloy. The developed composite coating resulted in a significant reduction in the corrosion rates. The results of this study show that it is possible to achieve more controlled corrosion rates of Mg-based implants towards patient-specific bone implant applications.
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Obradović, Darija, Milica Radan, Marija Popović-Nikolić, Slavica Oljačić i Katarina Nikolić. "THE MOLECULAR BASIS OF DRUG-PLASMA PROTEIN INTERACTION FOR CNS ACTIVE COMPOUNDS". W 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.375o.

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The human serum albumin (HSA) is well known for its extraordinary binding capacity for both endogenous and exogenous compounds, including a wide range of drugs. The goal of our investigation was to evaluate the distribution process for 15 CNS active compounds. The drug-plasma protein interaction was evaluated under simulative physiological conditions on the HSA-based stationary phase by using the mixture of Sørensen phosphate buffer (pH 7.40) and acetonitrile modifier as a mobile phase (84:16 v/v). The retention parameters (k) were used to approximate the % of protein-binding by calculating the P(%) values. The results obtained through this study demonstrated that the constitutional properties (e.g. number of total bonds, atoms, carbon atoms) and lipophilicity have a strong positive impact on the HSA-binding affinity. The coefficient of diffusion has a negative impact, while the atoms and sites available for the CYP450 oxidation showed the most significant correlation (r = 0.92). This study provides a basis for further in vitro chromatographical investigations of drug-HSA interaction for CNS active compounds. The correlation between obtained retention data and the availability to enzymes oxidation indicates the application of the tested system in the assessment of the metabolic degradation profile of CNS related drugs.
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Ryu, Jae-Joong, i Pranav Shrotriya. "Roughness Evolution of Metallic Implant Surfaces Under Contact Loading and Nanoscale Chemical Etching: Influence of Surface Roughness and Contact Loading". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206321.

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Metallic materials are chosen for orthopedic implants because of their high load-bearing capacity, low cost and low wear rates. However, repeated contact loading at taper-locked or clamped of metallic implant interfaces results in formation of soluble and particulate debris due to the simultaneous action of mechanical loading and electrochemical reactions in the corrosive physiological environment [1–3]. Previous work on understanding metallic implant surface damage due to mechanical load assisted dissolution has run the gamut from examination of retrieved implants [4, 5, 6 ] to in-vitro implant scale experiments (see for instance [7] and references in review articles [2, 5]). Results of these studies indicate that there is a synergistic interaction of mechanical loading and electrochemical oxidation i.e. material degradation is accelerated by the combined effects of contact loading and corrosion.
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Liu, Lingyi, i Ozan Ciftci. "Extrusion 3D Printing and Oxidative Stability of High-oil-content Printing Paste Formulated with Waxes-based Oleogels". W 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/otph5794.

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Abstract: Saturated fats exhibit more desirable properties for 3D food printing compared with liquid oils. However, increasing consumption of saturated fats is highly related to the pathogenesis of multiple diseases and physiological disorders. Wax-based oleogels as potentially healthier alternatives have drawn attention in food technology and industry recently. Inspired by the potential opportunities offered by sorghum as a natural wax source, the first objective of this study was to investigate the potential of three types of sorghum waxes, namely, sorghum bran wax, sorghum DDGS wax (SDW), and sorghum kernel wax, as an oleogelator. All three sorghum waxes showed good gelation properties with minor differences. Fast cooling rate and ultrasonic treatment favored the oil-gelling capacity and reduced oil loss by decreasing the crystal size. X-ray diffraction results indicated that all sorghum wax oleogels demonstrated a hexagonal symmetry and β’ crystals. Faster cooling rate resulted in an earlier onset of crystallization and ultrasonic treatment narrowed the melting range. Oxidation of fish oil in the sorghum wax oleogels was delayed considerably compared to free fish oil, while SDW generated the most stable oleogels. Next, four natural waxes were used to print on an extrusion-based 3D printer to explore the effect of wax-based oleogels on printability and post-printing properties. Results indicated that all wax-based oleogels showed excellent printability with the wax concentration under 6%, except SDW under 4%. The rheological properties of printing pastes were impaired with the increased wax concentration, while the higher wax concentration promoted the physical stability for beeswax and candelilla wax oleogel pastes. 6% beeswax oleogels exhibited the optimal capacity to keep the deposited shape lasting to 53 days. The wax with different concentrations in the oleogels displayed various effects on the oil-controlling capacity. Oxidative stability showed that wax-based oleogels displayed oxidative protection for the fish oil printed products.
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Yun, Yeoheung, Yongseok Jang, Juan Wang, Zhongyun Dong, Vesselin Shanov, Jagannathan Sankar, Youngmi Koo, Leon White i Boyce Collins. "Biodegradable Magnesium Implant: In Vivo and In Vitro Convergence". W ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39262.

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In recent years, magnesium alloys have emerged as possible biodegradable implant material. A fundamental understanding of the nature of magnesium corrosion and the ability to control this process in vivo is critical to advancing the case for clinical use of magnesium based biomaterials. The biodegradation of magnesium is fundamentally linked to studies of its corrosion, which is dependent on the interfacing dynamics between the material and its environment. Thus, it is required to confirm what variable differentiate the corrosion behavior between in vitro and in vivo before optimizing and standardizing of in vitro test. This study was conducted to understand the biodegradation behavior of commercial AZ31 and Mg-Zn-Ca alloys with plasma electrolyte oxidation (PEO) under various biological environments using in vivo and in vitro testing methods mimicking in vivo physiological environment. This study is focused on the effect of Zn element concentration and PEO coating for magnesium alloys, and the correlation between the in vivo and in vitro in terms of corrosion rate, types of corrosion and corrosion product formation.
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Wake, Amanda K., Geeta Datta, Mayakonda N. Palgunachari, Vinod K. Mishra, G. M. Anantharamaiah i C. Roger White. "Apolipoprotein A-I Mimetic Peptide Retains Function After Oxidant Exposure". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-189660.

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Mechanical integrity of arteries is vital for maintaining compensatory mechanisms under physiologic conditions, and changes in vessel structure (and consequently, vessel mechanical properties) are hallmarks of the progression of pathologic states. Oxidative stress can (1) induce endothelial dysfunction by interfering with nitric oxide (NO) signaling pathways relevant to vasodilation/vasoconstriction of arteries, and (2) alter atherosclerotic plaque composition by oxidation of constituents or by interruption of reverse cholesterol transport from plaques.
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Bashkatova, V. G., i H. Prast. "THE ROLE OF OXIDATIVE STRESS IN MECHANISMS OF NEUROPHYSIOLOGICAL EFFECTS OF PSYCHOSTIMULANT DRUGS". W MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-17.

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Kostrova, G. N., S. I. Malyavskaya i A. V. Lebedev. "PARAMETERS OF OXIDATIVE STRESS IN VITAMIN D DEFICIENCY IN YOUNG PEOPLE LIVING IN THE ARCTIC REGION". W MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-44.

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Raporty organizacyjne na temat "Physiological oxidation"

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Steffens, John, Eithan Harel i Alfred Mayer. Coding, Expression, Targeting, Import and Processing of Distinct Polyphenoloxidases in Tissues of Higher Plants. United States Department of Agriculture, listopad 1994. http://dx.doi.org/10.32747/1994.7613008.bard.

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Polyphenol oxidase (PPO) catalyzes the oxidation of phenols to quinones at the expense of O2. PPOs are ubiquitous in higer plants, and their role in oxidative browning of plant tissues causes large annual losses to food production. Despite the importance of PPOs to agriculture, the function(s) of PPOs in higher plants are not understood. Among other roles, PPOs have been proposed to participate in aspects of chloroplast metabolism, based on their occurrence in plastids and high Km for O2. Due to the ability of PPO to catalyze formation of highly reactive quinones, PPOs have also been proposed to be involved in a wide array of defensive interactions with insect, bacterial, and fungal pests. Physiological and biochemical studies of PPO have provided few answers to the major problems of PPO function, subcellular localization, and biochemical properties. This proposal achieved the following major objectives: cloning of PPO cDNAs in potato and tomato; characterization of the tomato PPO gene family; antisense downregulation of the tomato PPO gene family; and reduction in post-harvest enzymic browning of potato through expression of antisense PPO genes under the control of tuber-specific promoters. In addition, we established the lumenal localization of PPO, characterized and clarified the means by which PPOs are imported and processed by chloroplasts, and provided insight into the factors which control localization of PPOs. This proposal has thereby provided fundamental advances in the understanding of this enzyme and the control of its expression.
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Pesis, Edna, Elizabeth J. Mitcham, Susan E. Ebeler i Amnon Lers. Application of Pre-storage Short Anaerobiosis to Alleviate Superficial Scald and Bitter Pit in Granny Smith Apples. United States Department of Agriculture, styczeń 2013. http://dx.doi.org/10.32747/2013.7593394.bard.

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There is increased demand for high quality fruit produced and marketed with reduced chemical inputs to minimize toxic effects on human health and the environment. Granny Smith (GS) apple quality is reduced by two major physiological disorders, superficial scald and bitter pit (BP). These disorders cause great loss to apple growers worldwide. Superficial scald is commonly controlled by chemical treatments, mainly the antioxidant diphenylamine (DPA) and/or the ethylene action inhibitor, 1-methylcyclopropene (1–MCP). Both chemicals are ineffective in controlling bitter pit incidence. We proposed to investigate the beneficial use of non-chemical, abiotic stress with low O2 (LO2) applied for 10d at 20°C on GS apple fruit. During the project we expanded the treatment to more apple cultivars, Golden Delicious (GD) and Starking Delicious (SD) and another pome fruit, the pear. Apple and pear have similar physiological disorders that develop during cold storage and we examined if the LO2 treatment would also be effective on pear. Application of 0.5% LO2 atmosphere for 10d at 20°C or 500ppb 1-MCP at 20°C prior to cold storage at 0°C, was effective in reducing superficial scald in GS apple. Moreover, LO2 pretreatment was also effective in reducing bitter pit (BP) development in California GS and Israeli GD and SD apples The BP symptoms in GS from California were much more prominent, so the effect of LO2 was more dramatic than the effect on the Israeli cvs. GD and SD, nevertheless the LO2 treatment showed the same trend in all cultivars in reducing BP. The LO2 and 1-MCP -treated fruit exhibited lower levels of ethylene, - farnesene and its oxidation product, 6-methyl-5-hepten-2-one (MHO), as determined by SPME/GC-MS analysis. In addition, LO2 pretreatment applied to California Bartlett or Israeli Spadona pears was effective in reducing superficial scald, senescent scald and internal breakdown after 4 m of cold storage at 0°C. For GS apple, low-temperature storage resulted in oxidative stress and chilling injury, caused by increased production of superoxide anions which in turn led to the generation of other dangerous reactive oxygen species (ROS). Using confocal laser-scanning microscopy and H2O2 measurements of apple peel, we observed ROS accumulation in control fruit, while negligible amounts were found in LO2 and 1-MCP treated fruit. Gene-expression levels of ROS-scavenging enzymes were induced by the various pretreatments: catalase was induced by LO2 treatment, whereas Mn superoxide dismutase was induced by 1-MCP treatment. We assume that LO2 and 1-MCP pretreated fruit remained healthier due to reduced production of ethylene and reactive oxygen substances, such as MHO, during cold storage. The LO2-treated apple exhibited greener peel and firmer fruit after 6 m of cold storage, and the fruit had high crispiness leading to high taste preference. In both pear cultivars, the LO2 treatment led to a reduction in internal breakdown and browning around the seed cavity. We tested the LO2 pre-storage treatment on a semi-commercial scale that would be applicable to a small organic grower by sealing the fruit within the plastic field bins. The treatment was most effective with a continuous flow of nitrogen through the bins; however, a single 6 hour flush of nitrogen was also fairly effective. In addition, we determined that it was very important to have the oxygen levels below 0.5% for approximately 10 days to achieve good scald control, not counting the time required to reduce the oxygen concentration. Our LO2 technology has been proven in this project to be effective in reducing several physiological disorders developed in pome fruit during cold storage. We hope that our non-chemical treatment which is friendly to the environment will be used in the near future for the organic apple and pear industry. The next step should be an analysis of the cost-benefits and commercial feasibility.
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Shahak, Yosepha, i Donald R. Ort. Physiological Bases for Impaired Photosynthetic Performance of Chilling-Sensitive Fruit Trees. United States Department of Agriculture, maj 2001. http://dx.doi.org/10.32747/2001.7575278.bard.

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Chilling-sensitivity is an important agricultural problem in both the U.S. and Israel. Most research attention has focused so far on herbaceous crop plants, even though the problem is also acute in the fruit tree industry. Under BARD funding we made substantial progress in identifying the mechanisms involved in the disruption of photosynthesis following a chill in mango. Our investigation with fruit trees has been substantially accelerated by drawing on our knowledge and experience with herbaceous crops. The four original research objectives, focused or discovering the underlying mechanisms of chill-induced inhibition of photosynthesis in fruit trees, and the main achievements are listed below. [1] Separating stomatal from non-stomatal components of chilling on photosynthesis in fruit trees. We found evidence that the dark chill-induced inhibition of photosynthesis in mango was E combination of both stomatal and mesophyll components. [2] Differentiating photo damage from light-induced photo protection of photosystem II (PSII). Dark chilling exacerbate high light photoinhibition, as a result of primary inhibition in the carbor reduction cycle. Nevertheless, in Israeli orchards we observed chronic photoinhibition of PSII photochemistry in the winter. This photo damage was reversible over a few days if sunlight was attenuated with filters or night temperature rose. Practical implications of this finding deserve further investment. Additional achievement was the development of a new biophysical tool to study macro-structural changes of LHCII particles in intact, attached leaves. [3] Determine the role of oxidative stress in the dark-chilling-induced inhibition, with emphasis on oxygen radical scavenging, lipid peroxidation and redox-controlled carbon-cycle enzymes. We found an increase in lipid peroxidation following a dark chill, and partial protective effects or an antioxidant. However, the photoinhibition observed in mango orchards in Israel during the winter did not appear to be a general oxidative stress. [4] Investigate whether chilling interferes with the diurnal and circadian rhythm of gene expression of key photosynthetic proteins as has been shown for chilling-sensitive crop plants. The results indicated that most of the circadian rhythm in photosynthesis was due to reduced lea: internal CO2 concentrations during the subjective night, as a result of rhythmic stomatal closure Chilling-induced interference with circadian timing in mango, does not play the central role in chilling inhibition of photosynthesis that has previously been demonstrated in certain chilling sensitive herbaceous plants. Practical implications of the research achievements are feasible, but require few more years of research.
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Horwitz, Benjamin, i Barbara Gillian Turgeon. Secondary Metabolites, Stress, and Signaling: Roles and Regulation of Peptides Produced by Non-ribosomal Peptide Synthetases. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696522.bard.

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Fungal pathogens of plants produce a diverse array of small molecules. Often referred to as secondary metabolites because they were thought to be dispensable for basic functions, they may indeed have central roles as signals for the fungal cell, and in interactions with the host. We have identified more than a dozen genes encoding nonribosomal peptide synthetases (NPS) in Cochliobolusheterostrophus, the agent of southern corn leaf blight. The aim of this project was to identify roles of these genes in stress responses and signaling. The first objective was to test a complete collection of C. heterostrophus nonribosomal peptide synthetase (NRPS)-encoding gene deletion mutant and wildtype (WT) strains for sensitivity to various agents of oxidative (ROS) and nitrosative (RNOS) stress, in vitro. The second objective and next step in this part of the project was to study the relevance of sensitivity to ROS and RNOS in the host pathogen interaction, by measuring the production of ROS and RNOS in planta, when plants are inoculated with wild type and mutant strains. A third objective was to study expression of any genes shown to be involved in sensitivity to ROS or RNOS, in vitro and in planta. Another objective was to determine if any of the genes involved in oxidative or nitrosative stress responses are regulated by components of signal transduction pathways (STP) that we have identified and to determine where mechanisms overlap. Study of the collection of nps mutants identified phenotypes relevant for virulence, development and oxidative stress resistance for two of the genes, NPS2 and NPS6. Mutants in genes related to RNOS stress have no virulence phenotypes, while some of those related to ROS stress have reduced virulence as well as developmental phenotypes, so we focused primarily on ROS stress pathways. Furthermore, the identification of NPS2 and NPS6 as encoding for NRPS responsible for siderophore biosynthesis lent a new focus to the project, regulation by Fe. We have not yet developed good methods to image ROS in planta and work in this direction is continuing. We found that NPS6 expression is repressed by Fe, responding over the physiological Fe concentration range. Studying our collection of mutants, we found that conserved MAPK and G protein signal transduction pathways are dispensable for Fe regulation of NPS6, and initiated work to identify other pathways. The transcription factor SreA is one candidate, and is responsible for part, but not all, of the control of NPS6 expression. The results of this project show that the pathogen contends with oxidative stress through several signaling pathways. Loss of the siderophore produced by Nps6 makes the fungus sensitive to oxidative stress, and decreases virulence, suggesting a central role of the ability to sequester and take up extracellular iron in the host-pathogen interaction. Siderophores, and manipulation of Fe levels, could be targets for new strategies to deal with fungal pathogens of maize and other plants.
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Watkins, Chris B., Susan Lurie, Amnon Lers i Patricia L. Conklin. Involvement of Antioxidant Enzymes and Genes in the Resistance Mechanism to Postharvest Superficial Scald Development. United States Department of Agriculture, grudzień 2004. http://dx.doi.org/10.32747/2004.7586539.bard.

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The objective of this research project was to evaluate the involvement of antioxidant enzymes and genes in the resistance mechanism to postharvest superficial scald development using two primary systems: 1. Resistant and susceptible progenies of an apple cross between a scald resistant crab apple, ‘White Angel’ and a scald susceptible cultivar, ‘Rome Beauty’; 2. Heat-treatment of ‘Granny Smith’, which is known to reduce scald development in this cultivar. In 2002 we asked for, and received (October 14), permission to revise our initial objectives. The US side decided to expand their results to include further work using commercial cultivars. Also, both sides wanted to include an emphasis on the interaction between these antioxidant enzymes and the á-farnesene pathway, with the cooperation of a third party, Dr. Bruce Whitaker, USDA-ARS, Beltsville. Background: Superficial scald is a physiological storage disorder that causes damage to the skin of apple and pear fruit. It is currently controlled by use of an antioxidant, diphenylamine (DPA), applied postharvest by drenching or dips, but concern exists about such chemical usage especially as it also involves application of fungicides. As a result, there has been increased emphasis on understanding of the underlying mechanisms involved in disorder development. Our approach was to focus on the oxidative processes that occur during scald development, and specifically on using the two model systems described above to determine if the levels of specific antioxidants and/or antioxidant enzyme activities correlated with the presence/absence of scald. It was hoped that information about the role of antioxidant-defense mechanisms would lead to identification of candidate genes for future transgenic manipulation. Major conclusions, solutions, achievements: Collectively, our results highlight the complexity of superficial scald developmental processes. Studies involving comparisons of antioxidant enzyme activities in different crab apple selection, commercial cultivars, and in response to postharvest heat and 1-methylcyclopropene (1-MCP) treatments, show no simple direct relationships with antioxidant contents and susceptibility of fruit to scald development. However, a correlative relationship was found between POX activity or isoenzyme number and scald resistance in most of the studies. This relationship, if confirmed, could be exploited in breeding for scald resistance. In addition, our investigations with key genes in the á-farnesenebiosynthetic pathway, together with antioxidant processes, are being followed up by analysis of exposed and shaded sides of fruit of cultivars that show different degrees of scald control by 1-MCP. These data may further reveal productive areas for future research that will lead to long term control of the disorder. However, given the complexity of scald development, the greatest research need is the production of transgenic fruit with down-regulated genes involved in á- farnesene biosynthesis in order to test the currently popular hypothesis for scald development.
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Sionov, Edward, Nancy Keller i Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, styczeń 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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