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Results for “Redox adaptation”

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At least 127 records · Page 7Linked to original sources

PubMed2005

Sleep-disordered breathing and cerebrovascular disease: a mechanistic approach.

The observations described in this article point to the existence of increased oxidative stress and systemic inflammation in sleep apnea and have paved the way for establishing sleep apnea as an independent risk factor for cardio- and cerebrovascular morbidities. The proposed course of events is summarized in Fig. 1. It is suggested that hypoxia/reoxygenation,characteristic of sleep apnea, promotes the formation of ROS, particularly during the reoxygenation period, and can be deleterious to cells and tissues. ROS, however, regulate the activation of critical transcription factors that are redox sensitive, resulting in increased expression of sets of genes that encode proteins essential to adaptation to hypoxia (via hypoxia inducible factor I [hypoxia inducible factor-la]). Yet, redox-sensitive transcription factors (NFKB and AP-1) that elicit inflammatory pathways also are activated, thereby affecting inflammatory and immune responses by promoting activation of endothelial cells, leukocytes, and platelets. These activated cells express adhesion molecules and proinflammatory cytokines that may lead to endothelial injury and dysfunction and consequently to the development of cardio- and cerebrovascular morbidities. These may be exaggerated in patients who have sleep apnea in response to the intermittent hypoxia.

C-Reactive Protein↗

PubMedDate not supplied

Metabolic oxidation/reduction reactions and cellular responses to ionizing radiation: a unifying concept in stress response biology.

Exposure of eukaryotic cells to ionizing radiation (IR) results in the immediate formation of free radicals that last a matter of milliseconds. It has been assumed that the subsequent alterations in multiple intracellular processes following irradiation is due to the initial oxidative damage caused by these free radicals. However, it is becoming increasingly clear that intracellular metabolic oxidation/reduction (redox) reactions can be affected by this initial IR-induced free radical insult and may remain perturbed for minutes, hours, or days. It would seem logical that these cellular redox reactions might contribute to the activation of protective or damaging processes that could impact upon the damaging effects of IR. These processes include redox sensitive signaling pathways, transcription factor activation, gene expression, and metabolic activities that govern the formation of intracellular oxidants and reductants. The physiological manifestations of these radiation-induced alterations in redox sensitive processes have been suggested to contribute to adaptive responses, bystander effects, cell cycle perturbations, cytotoxicity, heat-induced radiosensitization, genomic instability, inflammation, and fibrosis. While a great deal is known about the molecular changes associated with the initial production of free radicals at the time of irradiation, the contribution of perturbations in redox sensitive metabolic processes to biological outcomes following exposure to IR is only recently becoming established. This review will focus on evidence supporting the concept that perturbations in intracellular metabolic oxidation/reduction reactions contribute to the biological effects of radiation exposure as well as new concepts emerging from the field of free radical biology that may be relevant to future studies in radiobiology.

Animals↗

PubMed2006

Crystal structures of a poxviral glutaredoxin in the oxidized and reduced states show redox-correlated structural changes.

Glutaredoxins act as reducing agents for the large subunit of ribonucleotide reductase (R1) in many prokaryotes and eukaryotes, including humans. The same relationship has been proposed for the glutaredoxin and R1 proteins expressed by all orthopoxviruses, including vaccinia, variola, and ectromelia virus. Interestingly, the orthopoxviral proteins share 45% and 78% sequence identity with human glutaredoxin-1 (Grx-1) and R1, respectively. To study structure-function relationships of the vertebrate Grx-1 family, and reveal potential viral adaptations, we have determined crystal structures of the ectromelia virus glutaredoxin, EVM053, in the oxidized and reduced states. The structures show a large redox-induced conformational rearrangement of Tyr21 and Thr22 near the active site. We predict that the movement of Tyr21 is a viral-specific adaptation that increases the redox potential by stabilizing the reduced state. The conformational switch of Thr22 appears to be shared by vertebrate Grx-1 and may affect the strictly conserved Lys20. A crystal packing-induced structural change in residues 68-70 affects the GSH-binding loop, and our structures reveal a potential interaction network that connects the GSH-binding loop and the active site. EVM053 also exhibits a novel cis-proline (Pro53) in a loop that has been shown to contribute to R1-binding in Escherichia coli Grx-1. The cis-peptide bond of Pro53 may be required to promote electrostatic interactions between Lys52 and the C-terminal carboxylate of R1. Finally, dimethylarsenite was covalently attached to Cys23 in one reduced EVM053 structure and our preliminary data show that EVM053 has dimethylarsenate reductase activity.

Animals↗

PubMedDate not supplied

Redox regulation of angiotensin II signaling in the heart.

A large number of studies have demonstrated the role of angiotensin II in cardiac preconditioning against ischemic reperfusion injury. Generally, angiotensin II is a detrimental factor for the heart, and its inhibition with an ACE inhibitor provides cardioprotection. This review provides an explanation for such paradoxical behavior of angiotensin II. Angiotensin II can potentiate the induction of the expression of a variety of redox-sensitive factors including p38 MAPK, JNK and Akt, IGF-IR, EGF-R, and HO-1 as well as redox-regulated genes and transcription factors such as NFkappaB. It becomes increasingly apparent that during the earlier phase, the heart attempts to adapt itself against the detrimental effects of angiotensin II by upregulating several cardioprotective genes and proteins. These genes and proteins are redox-regulated and the antioxidants or ROS scavengers block their expressions. Interestingly, an identical pattern of cardioprotective proteins and genes are expressed in the preconditioned heart, which are also inhibited with ROS scavengers. It is tempting to speculate that the induction of the expression of the redox-sensitive cardioprotective proteins is the results of adaptation of the heart against the oxidative stress resulting from angiotensin II; and preconditioning is the net result of harnessing its own protection during ischemic and/or oxidative stress through its ability to trigger redox signaling.

Angiotensin II↗

PubMed2000

Differential effects of chilling-induced photooxidation on the redox regulation of photosynthetic enzymes.

Photosynthesis in plant species that are evolutionarily adapted for growth in warm climates is highly sensitive to illumination under cool conditions. Although it is well documented that illumination of these sensitive species under cool conditions results in the photosynthetic production of reactive oxygen molecules, the underlying mechanism for the inhibition of photosynthesis remains uncertain. Determinations of chloroplast fructose-1,6-bisphosphatase and sedoheptulose-1,7-bisphosphatase activity showed that the light-dependent, reductive activation of these key carbon reduction cycle enzymes was substantially inhibited in tomato (Lycopersicon esculentum) following illumination at 4 degrees C. However, other chloroplast enzymes also dependent on thioredoxin-mediated reductive activation were largely unaffected. We performed equilibrium redox titrations to investigate the thermodynamics of the thiol/disulfide exchange between thioredoxin f and the regulatory sulfhydryl groups of fructose-1,6-bisphosphatase, sedoheptulose-1,7-bisphosphatase, phosphoribulokinase, NADP-glyceraldehyde phosphate dehydrogenase, and the chloroplast ATPsynthase. We determined that the redox midpoint potentials for the regulatory sulfhydryl groups of the various enzymes spanned a broad range ( approximately 50 mV at pH 7. 9). The electron-sharing equilibria among thioredoxin f and its target enzymes largely explained the differential effects of photooxidation induced at low temperature on thioredoxin-mediated activation of chloroplast enzymes in tomato. These results not only provide a plausible mechanism for the low-temperature-induced inhibition of photosynthesis in this important group of plants, but also provide a quantitative basis to evaluate the influence of thioredoxin/target enzyme electron-sharing equilibria on the differential activation and deactivation kinetics of thioredoxin-regulated chloroplast enzymes.

ATP Synthetase Complexes↗

PubMed2003

Molecular mechanisms of iron uptake in fungi.

Fungi, like all free-living organisms, are in competition for limiting nutrients. In accumulating iron, fungi are faced also with a trace metal whose aqueous and redox chemistry make it both relatively bio-unavailable and strongly cytotoxic. Successful adaptation to this environmental context has provided fungi with an iron uptake strategy that has three features: it relies on redox cycling to enhance iron bio-availability and reduce iron cytotoxicity; it includes both high- and low-affinity pathways that are mechanistically distinct; and it is autoregulating so as to maintain intracellular iron homeostasis. Using Saccharomyces cerevisiae as a paradigm, this review summarizes current knowledge about the four pathways by which this yeast accumulates iron. These four pathways include: siderophore iron accumulation; high affinity iron uptake via an iron permease; and two lower affinity uptake pathways through relatively non-specific divalent metal ion transporters. All of these four pathways are directly or indirectly dependent on the activity of metalloreductase activity expressed extracellularly on the plasma membrane. A variety of experimental and genomics data indicate that this resourcefulness is shared by many, if not most, fungi. On the other hand, while the autoregulation of iron metabolism in Baker's yeast is well-understood, little is known about the apparent homeostatic mechanisms in these other yeasts and fungi. The integration of these multiple uptake mechanisms and their regulation into over-all iron homeostasis in yeast concludes this brief review.

Ascomycota↗

PubMed1988

Amperometric enzyme-amplified immunoassays.

Enzyme-amplified immunoassays have been adapted for electrochemical measurement, using an NAD+/NADH redox cycle coupled to an electrode via the active site of diaphorase. Two amperometric methods are described, the first employs an organic conducting salt electrode, NMP+/TCNQ-; the second a platinum wire with ferricyanide as electron transfer mediator. In an immunoenzymometric assay for human prostatic acid phosphatase the sensitivities of the electrochemical methods were comparable to that achieved with the existing optical technique, but the dynamic range of the electrochemical assays was increased by at least two orders of magnitude. It is proposed that electrochemical enzyme-amplified immunoassays may eventually replace their optical counterparts.

Acid Phosphatase↗

PubMed2004

Coenzyme Q10 changes are associated with metabolic syndrome.

BACKGROUND: The purpose of this study was to determine whether coenzyme Q10 (CoQ) concentrations and redox status are associated with components of the metabolic syndrome. METHODS: This is a cross-sectional survey of 223 adults (28-78 years), who were drawn from the ongoing Princeton Follow-up Study in greater Cincinnati. Individuals were assessed for measures of fatness, blood pressure, glucose, lipid profiles, C-reactive protein (CRP), reduced CoQ (ubiquinol), oxidized CoQ (ubiquinone), total CoQ and CoQ redox ratio (ubiquinol/ubiquinone). RESULTS: After adjusting for age, sex and race, we found that total CoQ, ubiquinol and CRP levels are significantly increased in metabolic syndrome. Comparison of minimal risk and high-risk metabolic syndrome groups indicates an increased CoQ redox ratio in the high risk group (p<0.05). Step-wise logistic regression analysis, using age, sex, race, (ln)CRP, total cholesterol, LDL, ubiquinol, ubiquinone and total CoQ as predictors, shows that only age (p=0.001), total CoQ adjusted for plasma lipids (p<0.0001) and (ln)CRP (p<0.005) were significant predictors of metabolic syndrome. CONCLUSIONS: The presence of metabolic syndrome components are associated with increased plasma total CoQ and ubiquinol concentrations after adjusting for age, sex and race. An increase in CoQ redox ratio may indicate a gender-specific adaptive response to oxidative stress in females, but not males.

Adult↗

PubMed2004

Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis.

Ferric nitrilotriacetate (Fe-NTA) induces oxidative renal damage leading to a high incidence of renal cell carcinoma (RCC) in rats. Differential display analysis of such RCCs revealed elevated expression of annexin 2 (Anx2), a substrate for kinases and a receptor for tissue-type plasminogen activator and plasminogen. We conducted this study to clarify the significance of Anx2 in Fenton reaction-based carcinogenesis. Messenger RNA and protein levels of Anx2 were increased time-dependently in the rat kidney after Fe-NTA administration as well as in LLC-PK1 cells after exposure to H2O2. The latter was inhibited by pretreatment with N-acetylcysteine, pyrrolidine dithiocarbamate or catalase. Immunohistochemistry revealed negligible staining in the normal renal proximal tubules, but strong staining in regenerating proximal tubules, karyomegalic cells and RCCs. Metastasizing RCCs showed higher Anx2 protein levels. Anx2 was phosphorylated at serine and tyrosine residues in these cells and coimmunoprecipitated with phosphorylated actin. Overexpression of Anx2 induced a higher cell proliferation rate in LLC-PK1 cells. In contrast, a decrease in proliferation leading to apoptosis was observed after Anx2 antisense treatment to cell lines established from Fe-NTA-induced RCCs. These results suggest that Anx2 is regulated by redox status, and that persistent operation of this adaptive mechanism plays a role in the proliferation and metastasis of oxidative stress-induced cancer.

Animals↗

PubMed2000

Eukaryotically encoded and chloroplast-located rubredoxin is associated with photosystem II.

We analyzed a eukaryotically encoded rubredoxin from the cryptomonad Guillardia theta and identified additional domains at the N- and C-termini in comparison to known prokaryotic paralogous molecules. The cryptophytic N-terminal extension was shown to be a transit peptide for intracellular targeting of the protein to the plastid, whereas a C-terminal domain represents a membrane anchor. Rubredoxin was identified in all tested phototrophic eukaryotes. Presumably facilitated by its C-terminal extension, nucleomorph-encoded rubredoxin (nmRub) is associated with the thylakoid membrane. Association with photosystem II (PSII) was demonstrated by co-localization of nmRub and PSII membrane particles and PSII core complexes and confirmed by comparative electron paramagnetic resonance measurements. The midpoint potential of nmRub was determined as +125 mV, which is the highest redox potential of all known rubredoxins. Therefore, nmRub provides a striking example of the ability of the protein environment to tune the redox potentials of metal sites, allowing for evolutionary adaption in specific electron transport systems, as for example that coupled to the PSII pathway.

Biological Transport↗

PubMed2006

South-seeking magnetotactic bacteria in the Northern Hemisphere.

Magnetotactic bacteria contain membrane-bound intracellular iron crystals (magnetosomes) and respond to magnetic fields. Polar magnetotactic bacteria in vertical chemical gradients are thought to respond to high oxygen levels by swimming downward into areas with low or no oxygen (toward geomagnetic north in the Northern Hemisphere and geomagnetic south in the Southern Hemisphere). We identified populations of polar magnetotactic bacteria in the Northern Hemisphere that respond to high oxygen levels by swimming toward geomagnetic south, the opposite of all previously reported magnetotactic behavior. The percentage of magnetotactic bacteria with south polarity in the environment is positively correlated with higher redox potential. The coexistence of magnetotactic bacteria with opposing polarities in the same redox environment conflicts with current models of the adaptive value of magnetotaxis.

Colony Count, Microbial↗

PubMed2003

Redox control, redox signaling, and redox homeostasis in plant cells.

Redox chemistry is a key feature of life. Oxidized substrates are reduced to synthesize functional molecules; reduced substrates are oxidized for energy supply. In addition, cells must fight against uncontrolled oxidation of essential constituents, a process that continuously occurs in an atmosphere of 21% O2. The redox situation is further complicated in plants with their highly reactive photosynthetic metabolism. To this end it is now well established that redox regulation is a central element in adjusting plant metabolism and development to the prevailing environmental conditions. This review introduces general redox chemistry and the main components of the cellular redox network, namely pyridine nucleotides, ascorbate, glutathione, lipoic acid, tocopherol, thioredoxins, glutaredoxins, peroxiredoxins, and other thiol proteins. Examples for redox sensing, transduction, redox-regulated enzymes and transcription, and the function of regulatory circuits are presented. Emphasis is placed on redox regulation of photosynthesis, which is the best understood metabolism governed by redox control on essentially all levels, ranging from gene transcription to translation, assembly and turnover, as well as short-term adaptation by state transition and enzyme activity. Increasing evidence shows the importance of redox regulation in the context of transport, plant development, and programmed cell death.

Feedback, Physiological↗

PubMed2006

Expression profiling and local adaptation of Boechera holboellii populations for water use efficiency across a naturally occurring water stress gradient.

We studied the physiological basis of local adaptation to drought in Boechera holboellii, a perennial relative of Arabidopsis thaliana, and used cDNA-AFLPs to identify candidate genes showing differential expression in these populations. We compared two populations of B. holboellii from contrasting water environments in a reciprocal transplant experiment, as well as in a laboratory dry-down experiment. We continuously measured the water content of soils using time domain reflectometery (TDR). We compared populations for their water use efficiency (WUE), root/shoot ratios (R:S) and leaf mass per unit area (LMA) in the field and in the laboratory, and identified candidate genes that (i) responded plastically to water stress and (ii) were differentially expressed between the two populations. Genotypes from the drier site had higher WUE, which was attributable to a large reduction in transpirational water loss. The xeric-adapted population also had increased investment in root biomass and greater leaf mass per unit area. Reciprocal transplants in the field had significantly greater survival in their native habitat. In total, 450 cDNA-AFLP fragments showed significant changes between drought and control treatments. Furthermore, some genes showed genotype (population)-specific patterns of up- or down-regulation in response to drought. Three hundred cDNA-AFLP bands were sequenced leading to the identification of cDNAs coding for proteins involved in signal transduction, transcriptional regulation, redox regulation, oxidative stress and pathways involved in stress adaptation. Some of these proteins could contribute a physiological advantage under drought, making them potential targets for natural selection.

Brassicaceae↗

PubMedDate not supplied

Thioredoxin target proteins in chloroplast thylakoid membranes.

In recent years, impressive progress has been made in the identification of thioredoxin-linked proteins. However, due to technical difficulties inherent in working with hydrophobic proteins, identifications so far have been restricted to proteins in the soluble fraction. Thus, our knowledge of redox regulated membrane proteins is quite limited. To gain information in this area, the authors have applied an adaptation of the approach based on the fluorescent thiol probe monobromobimane (mBBr) to identify redox-linked proteins of chloroplast thylakoids. By application of this procedure, 14 potential membrane-bound thioredoxin target proteins were identified, including seven new candidates functional in processes associated with photosynthetic electron flow, ATP synthesis, and Photosystem II/Photosystem I state transitions.

Bridged Bicyclo Compounds↗

PubMed2000

Exercise, oxidative stress and ageing.

Skeletal muscle has the unique ability to increase the rate of oxygen usage during contraction. This has led several workers to suggest that by-products of this increased oxygen consumption, oxygen-derived free radicals, may be primarily responsible for exercise-induced damage to skeletal muscle. However, because of this rapidly changing redox state, skeletal muscle has developed a number of different endogenous mechanisms which adapt rapidly following a period of exercise. These include numerous structural and biochemical changes such as increased muscle activity of antioxidant enzymes and content of stress or heat shock proteins (HSPs). This adaptation is associated with protection against the potentially damaging effects of a second period of exercise. In addition, we have recently demonstrated a significant increase in free radical production during a period of nondamaging exercise, which is rapidly followed by a significant increase in the expression of antioxidant enzymes and HSPs, suggesting that a change in redox state of the muscle may act as signal for adaptation.

Adaptation, Physiological↗

PubMed2002

Interactions between biosynthesis, compartmentation and transport in the control of glutathione homeostasis and signalling.

Glutathione has numerous roles in cellular defence and in sulphur metabolism. These functions depend or impact on the concentration and/or redox state of leaf glutathione pools. Effective function requires homeostatic control of concentration and redox state, with departures from homeostasis acting as signals that trigger adaptive responses. Intercellular and intracellular glutathione pools are linked by transport across membranes. It is shown that glutathione can cross the chloroplast envelope at rates similar to the speed of biosynthesis. Control of glutathione concentration and redox state is therefore due to a complex interplay between biosynthesis, utilization, degradation, oxidation/reduction, and transport. All these factors must be considered in order to evaluate the significance of glutathione as a signalling component during development, abiotic stress, or pathogen attack.

Aminoacyltransferases↗

PubMed1991

Unusual low reactivity of the water oxidase in redox state S3 toward exogenous reductants. Analysis of the NH2OH- and NH2NH2-induced modifications of flash-induced oxygen evolution in isolated spinach thylakoids.

The effect of redox-active amines NH2R (R = OH or NH2) on the period-four oscillation pattern of oxygen evolution has been analyzed in isolated spinach thylakoids as a function of the redox state Si (i = 0, ..., 3) of the water oxidase. The following results were obtained: (a) In dark-adapted samples with a highly populated S1 state, NH2R leads via a dark reaction sequence to the formal redox state "S-1"; (b) the reaction mechanism is different between the NH2R species; NH2OH acts as a one-electron donor, whereas NH2NH2 mainly functions as a two-electron donor, regardless of the interacting redox state Si (i = 0, ..., 3). For NH2NH2, the modified oxygen oscillation patterns strictly depend upon the initial ratio [S0(0)]/[S1(0)] before the addition of the reductant; while due to kinetic reasons, for NH2OH this dependence largely disappears after a short transient period. (c) The existence of the recently postulated formal redox state "S-2" is confirmed not only in the presence of NH2NH2 [Renger, G., Messinger, J., & Hanssum, B. (1990) in Current Research in Photosynthesis (Baltscheffsky, M., Ed.) Vol. 1, pp 845-848, Kluwer, Dordrecht] but also in the presence of NH2OH. (d) Activation energies, EA, of 50 kJ/mol were determined for the NH2R-induced reduction processes that alter the oxygen oscillation pattern from dark-adapted thylakoids. (e) Although marked differences exist between NH2OH and NH2NH2 in terms of the reduction mechanism and efficiency (which is about 20-fold in favor of NH2OH), both NH2R species exhibit the same order of rate constants as a function of the redox state Si in the nonperturbed water oxidase: kNH2R(S0) greater than kNH2R(S1) much less than kNH2R(S2) much greater than kNH2R(S3) The large difference between S2 and S3 in their reactivity toward NH2R is interpreted to indicate that a significant change in the electronic configuration and nuclear geometry occurs during the S2----S3 transition that makes the S3 state much less susceptible to NH2R. The implications of these findings are discussed with special emphasis on the possibility of complexed peroxide formation in redox state S3 postulated previously on the basis of theoretical considerations [Renger, G. (1978) in Photosynthetic Water Oxidation (Metzner, H., Ed.) pp 229-248, Academic Press, London].

Hydrazines↗

PubMed2000

Regulation of cardiomyocyte apoptosis by redox-sensitive transcription factors.

Reperfusion of ischemic myocardium results in apoptotic cell death and DNA fragmentation. Several transcription factors are known to regulate the apoptotic cell death. This study sought to examine the regulation of cardiomyocyte apoptosis by these transcription factors. Isolated working rat hearts were divided into six groups: control, 15 min ischemia, 60 min ischemia, 15 min ischemia followed by 2 h reperfusion, ischemic stress adaptation by subjecting the hearts to four cyclic episodes to 5 min ischemia, each followed by 10 min of reperfusion, and adaptation followed by 15 min ischemia and 2 h reperfusion. Redox-regulated transcription factors, NF kappa B and AP-1 and the expression of two anti- and pro-apoptotic genes, Bcl-2 and p53 were determined. The results demonstrated NF kappa B and AP-1 progressively and steadily increased as a function of the duration of ischemia. In the adapted heart, NF kappa B binding remained high while AP-1 binding was lowered to almost baseline value. The anti-oxidant gene, Bcl-2 was downregulated in the ischemic/reperfused heart, but upregulated in the preconditioned myocardium. Significant induction of the expression of p53 occurred after ischemia and reperfusion. Apoptotic cells were barely detected in the adapted myocardium which was subjected to the same ischemia/reperfusion protocol. The results demonstrate for the first time differential regulation of cardiomyocyte apoptosis by pro- and anti-apoptotic transcription factors and genes as a function of different durations of ischemia and reperfusion.

Animals↗