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At least 145 records · Page 8Linked to original sources

The kinetic behavior of P-700 during the induction of photosynthesis in algae.

The kinetics of P-700 were examined spectrophotometrically during the induction of photosynthesis in algae. A pronounced oscillation was observed in the redox level of P-700 upon illumination of dark-adapted cells. The dark adaptation required approximately 1 min. The oscillation may be described as an initial rapid oxidation reaching a peak at approx. 50 ms followed by complete reduction of the pool of P-700. A subsequent slower oxidation resulted in attainment of the final state around 1 s. The main features of the oscillation were qualitatively the same in a wide variety of algae. The modulation in redox level of P-700 required high intensity activation of both photosystems and was eliminated by pre-illumination of the cells with weak short wavelength light but not by longer wavelengths absorbed primarily by Photosystem I. We propose that the P-700 modulation is directly related to the fast redox changes in Photosystem II which occur during the induction of photosynthesis. Cells incubated with methyl viologen did not show the P-700 oscillation confirming the suggestion previously advanced that exhaustion of Photosystem I acceptor and kinetic limitations in the carbon reduction cycle partially control the fast phase of photosynthetic induction.

Bacteria↗

Studies on adaptation to adriamycin in cells pretreated with hydrogen peroxide.

Various investigations have reported the occurrence in bacterial and mammalian cells of an adaptive response to the toxic effects of oxidants or agents that cause oxidation via redox reactions. In our previous study, it was shown that several cell lines pretreated with a low dose of hydrogen peroxide (H2O2) exhibited an adaptive response to subsequent high doses of adriamycin (ADR), whereas other cell lines did not. Based on the observation that the cell lines utilized differed in their sensitivity towards adriamycin, we undertook the present investigation with the goal of evaluating possible relationships between the levels of antioxidant enzymes and sensitivity towards adriamycin. Another aim was to determine relationships between the inducibility of these enzymes and the occurrence of adaptation. We utilized African Green monkey kidney (V3), human embryo (CLV98), human melanoma (ME18), and Chinese hamster ovary (CHO) cell lines and experimentally developed adriamycin-resistant human melanoma (ME18/RN) and Chinese hamster ovary (CHO/RN) cell sublines. Cytotoxicity was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and trypan blue exclusion. The levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were determined in the same kind of experiment as that revealing the occurrence of adaptation. The rank order established for catalase activities was similar to that for sensitivity towards adriamycin. Aberrant increases in the tested enzymes were demonstrated in experimental groups of all kinds of cells. We conclude that in our cell systems catalase is a major determinant of adriamycin resistance. Whether the occurrence of the adaptive response under study is dependent on the contribution of catalase, itself dependent on the degree of resistance to the drug, is discussed.

Adaptation, Physiological↗

Transient binding of plastocyanin to its physiological redox partners modifies the copper site geometry.

The transient complexes of plastocyanin with cytochrome f and photosystem I are herein used as excellent model systems to investigate how the metal sites adapt to the changes in the protein matrix in transient complexes that are involved in redox reactions. Thus, both complexes from the cyanobacterium Nostoc sp. PCC 7119 (former Anabaena sp. PCC 7119) have been analysed by X-ray absorption spectroscopy. Our data are consistent with a significant distortion of the trigonal pyramidal geometry of the Cu coordination sphere when plastocyanin binds to cytochrome f, no matter their redox states are. The resulting tetrahedral geometry shows a shortening of the distance between Cu and the S(delta) atom of its ligand Met-97, with respect to the crystallographic structure of free plastocyanin. On the other hand, when plastocyanin binds to photosystem I instead of cytochrome f, the geometric changes are not significant but a displacement in charge distribution around the metal centre can be observed. Noteworthy, the electronic density around the Cu atom increases or decreases when oxidised plastocyanin binds to cytochrome f or photosystem I, respectively, thus indicating that the protein matrix affects the electron transfer between the two partners during their transient interaction.

Binding Sites↗

Flash-induced relaxation changes of the EPR signals from the manganese cluster and YD reveal a light-adaptation process of photosystem II.

By exposing photosystem II (PSII) samples to an incrementing number of excitation flashes at room temperature, followed by freezing, we could compare the Mn-derived multiline EPR signal from the S2 oxidation state as prepared by 1, 5, 10, and 25 flashes of light. While the S2 multiline signals exhibited by these samples differed very little in spectral shape, a significant increase of the relaxation rate of the signal was detected in the multiflash samples as compared to the S2-state produced by a single oxidation. A similar relaxation rate increase was observed for the EPR signal from Y(D*). The temperature dependence of the multiline spin-lattice relaxation rate is similar after 1 and 5 flashes. These data are discussed together with previously reported phenomena in terms of a light-adaptation process of PSII, which commences on the third flash after dark-adaptation and is completed after 10 flashes. At room temperature, the fast-relaxing, light-adapted state falls back to the slow-relaxing, dark-adapted state with t(1/2) = 80 s. We speculate that light-adaptation involves changes necessary for efficient continuous water splitting. This would parallel activation processes found in many other large redox enzymes, such as Cytochrome c oxidase and Ni-Fe hydrogenase. Several mechanisms of light-adaptation are discussed, and we find that the data may be accounted for by a change of the PSII protein matrix or by the light-induced appearance of a paramagnetic center on the PSII donor side. At this time, no EPR signal has been detected that correlates with the increase of the relaxation rates, and the nature of such a new paramagnet remains unclear. However, the relaxation enhancement data could be used, in conjunction with the known Mn-Y(D) distance, to estimate the position of such an unknown relaxer. If positioned between Y(D) and the Mn cluster, it would be located 7-8 A from the spin center of the S2 multiline signal.

Adaptation, Physiological↗

Oxygen sensing and oxidant/redox-related pathways.

What is the nature of the oxygen sensor(s) and how do organisms sense variations in oxygen? A progressive rise of oxidative stress due to the altered reduction-oxidation (redox) homeostasis appears to be one of the hallmarks of the processes that regulate gene transcription. Dynamic changes in oxygen homeostasis and its close association with redox equilibrium, therefore, constitute a signaling mechanism for the expression/activation of oxygenes. This variation subsequently regulates the compartmentalization and functioning of HIF-1alpha and NF-kappaB. In addition, oxygen-evoked regulation of HIF-1alpha and NF-kappaB is closely coupled with intracellular redox state, such that modulating redox equilibrium affects their responsiveness at the molecular level (expression/transactivation). Interestingly, are these particular transcription factors potential oxygen sensors? The basic components of the intracellular oxidative/redox machinery and its crucial regulation of oxygen- and redox-sensitive transcription factors may help understand the network of oxygen sensing mechanisms and redox-related pathways.

Adaptation, Physiological↗

Effect of gender differences and voluntary exercise on antioxidant capacity in rats.

The effects of gender difference and voluntary exercise on antioxidant capacity in rats were evaluated. The subjects were divided into two groups, physically active and sedentary. In the sedentary group, the level of hydroxyl radical in the liver was higher (P<0.001) in male rats than in female rats, however, in the physically active group, the level in male rats was lower (P<0.05) than in female rats. The levels of reduced glutathione (GSH) in physically active males and females were higher compared to those in the sedentary group. The physically active group also showed an increase in antioxidant enzymes, such as glutathione peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase activities. The level of liver GSH was higher in physically active females than in physically active males. For both groups, GPx and GR activities in females were significantly higher than in males. These results indicate that female rats have an intrinsically higher antioxidant capacity, which resulted in increased levels of GSH via the glutathione redox cycle and gamma-glutamyl cycle enzymes. The adaptation to altered antioxidant capacity, induced by physical activity, appeared to be affected by gender differences.

Animals↗

Carbohydrate cycling in micro-organisms: what can (13)C-NMR tell us?

The extension of (13)C-nuclear magnetic resonance (NMR) techniques to study cellular metabolism over recent years has provided valuable data supporting the occurrence, diversity and extent of carbon cycling in the carbohydrate metabolism of micro-organisms. The occurrence of such cycles, resulting from the simultaneous operation of different and sometimes opposite individual steps, is inherently related to the network organisation of cellular metabolism. These cycles are tentatively classified here as 'reversibility', 'metabolic' and 'substrate' cycles on the basis of their balance in carbon and cofactors. Current hypotheses concerning the physiological relevance of carbohydrate cycles are discussed in light of the (13)C-NMR data. They most likely represent system-level mechanisms for coherent and timely partitioning of carbon resources to fit with the various biosynthetic, energetic or redox needs of cells and/or additional strategies in the adaptive capacity of micro-organisms to face variation in environmental conditions.

Azotobacter vinelandii↗

Fiber optic surface fluorometry-reflectometry technique in the renal physiology of rats.

Most current knowledge on events in the mitochondria leading to acute renal failure originates from studies in which indirect methods were used. The disadvantage of these methods is that they cannot measure the turnover rate of various metabolites, and only one result per animal can be obtained. Chance et al. /9/ developed a method using optical techniques for continuously monitoring the fluorescence of intramitochondrial NADH, which has been applied mainly to the brain. This optical method has not yet been examined quantitatively in the kidney and no attempt has been made to adapt this method for routine measurement in kidney tissue. The purpose of this study was to adapt the surface fluorometry method for monitoring renal NADH redox state in situ, and to determine whether the hemodynamic artifacts involved in fluorometric studies of the renal surface in situ could be eliminated by using a correction factor. Another purpose was to understand the relationship between the changes in reflectance and blood volume in the rat kidney. This was achieved by measuring the reflectance after: a) blood exchange by FC-43 emulsion; b) intrarenal saline flush; c) occlusion of the renal vein, renal artery and reopening of the renal vein; d) calculation of the correlation between changes in kidney weight after renal artery occlusion, and the reflectance. Our results suggest that in the rat kidney, as opposed to the brain, a correction factor of 1:1 is not always applicable. This factor may vary between animals, and it is therefore necessary to adjust it electronically for each rat kidney. This observation contradicts the view suggesting a constant correction factor of 1:1 in the kidney. The results reported herein indicate that changes in the reflectance in the ischemic rat kidney are due to changes in blood volume. In conclusion, it seems that optical techniques for monitoring fluorescence are suitable for localized, continuous and non-invasive recording of tissue mitochondrial NADH redox states under various conditions in the rat kidney.

Animals↗

MpcT is the transducer for membrane potential changes in Halobacterium salinarum.

In Halobacterium salinarum mutants containing either of the light-driven ion pumps bacteriorhodopsin (H(+)) or halorhodopsin (Cl(-)) as their only retinal protein, a decrease of irradiance in the absence of respiration causes a phototactic response. The conversion of the causal event, a decrease of proton motive force across the cell membrane, into a reversal of flagellar motor rotational direction was expected to involve a transducer. Via deletion analysis of all 18 known and putative halobacterial transducer (htr) genes, we found that Htr14, a methylatable membrane-bound transducer lacking an extracellular domain, mediates the biological response, which includes adaptive methylation. Based on a minimal stimulus length of 200 ms and the determined cytoplasmic buffering capacity, we conclude that the change in the membrane potential (DeltaPsi), and not that of the internal pH, is the signal-generating event. Htr14 was therefore renamed to Membrane potential change Transducer, or MpcT. It is the first transducer for which the causative stimulus could be narrowed to a change in DeltaPsi, as opposed to a change in pH or cellular redox state.

Adaptation, Physiological↗

APE/Ref-1 and the mammalian response to genotoxic stress.

Human apurinic/apyrimidinic endonuclease/redox factor-1 (hAPE/Ref-1) is a multifunctional protein involved in the repair of DNA damaged by oxidative or alkylating compounds as well as in the regulation of stress inducible transcription factors such as AP-1, NF-kappaB, HIF-1 and p53. With respect to transcriptional regulation, both redox dependent and independent mechanisms have been described. APE/Ref-1 also acts as a transcriptional repressor. Recent data indicate that APE/Ref-1 negatively regulates the activity of the Ras-related GTPase Rac1. How these different physiological activities of APE/Ref-1 are coordinated is poorly understood. So far, convincing evidence is available that the expression of the APE/Ref-1 gene is inducible by oxidative stress and that overexpressed APE/Ref-1 protein protects cells against the genotoxic and cell killing effects of reactive oxygen species (ROS), whereas down-regulation sensitizes cells. Therefore, APE/Ref-1 can be considered to be part of an adaptive cellular response mechanism to oxidative genotoxic stress. The physiological relevance of increase of either the repair or redox activity of APE/Ref-1 for this adaptive response is unclear. Data will be shown that transfection of the truncated protein exhibiting either one of the activities provoked increase of resistance. Since APE/Ref-1 expression level and intracellular localization is variable in different types of tumors and frequently found to be different in non-malignant compared to the corresponding malignant human tissue, the protein is thought to be a diagnostic and prognostic tumor marker. Because of its involvement in DNA repair and apoptosis-related signaling mechanisms, APE/Ref-1 is also being discussed as a novel target for tumor-therapeutic approaches.

Amino Acid Sequence↗

Plasma membrane electron transport coupled to Na(+) extrusion in the halotolerant alga Dunaliella.

The halotolerant alga Dunaliella adapts to exceptionally high salinity and maintains low [Na(+)](in) at hypersaline solutions, suggesting that it possesses efficient mechanisms for regulating intracellular Na(+). In this work we examined the possibility that Na(+) export in Dunaliella is linked to a plasma membrane electron transport (redox) system. Na(+) extrusion was induced in Dunaliella cells by elevation of intracellular Na(+) with Na(+)-specific ionophores. Elevation of intracellular Na(+) was found to enhance the reduction of an extracellular electron acceptor ferricyanide (FeCN). The quinone analogs NQNO and dicumarol inhibited FeCN reduction and led to accumulation of Na(+) by inhibition of Na(+) extrusion. These inhibitors also diminished the plasma membrane potential in Dunaliella. Anaerobic conditions elevated, whereas FeCN partially decreased intracellular Na(+) content. Cellular NAD(P)H level decreased upon enhancement of plasma membrane electron transport. These results are consistent with the operation of an electrogenic NAD(P)H-driven redox system coupled to Na(+) extrusion in Dunaliella plasma membrane. We propose that redox-driven Na(+) extrusion and recycling in Dunaliella evolved as means of adaptation to hypersaline environments.

Cell Membrane↗

CD81 associates with 14-3-3 in a redox-regulated palmitoylation-dependent manner.

As a member of the tetraspanin superfamily of proteins, CD81 has been linked to a number of biologic functions including cellular proliferation, differentiation, activation, and degranulation. As a co-receptor for hepatitis C virus, and a requirement for hepatocytes for infectivity of human Plasmodium falciparum and rodent P. yoelii sporozoite infectivity, CD81 may also play a vital role in pathology. Despite the importance of CD81 in multiple cellular functions, the molecular mechanism of action of CD81 in these processes has remained elusive. Here we report an association between CD81 and the epsilon isoform of 14-3-3, a serine/threonine-binding intracellular signaling protein. Furthermore, we provide evidence that in human, this association is influenced by the palmitoylation state of the CD81 cytoplasmic tails. We have generated a series of CD81 cysteine mutants to identify palmitoylated intracellular motifs of CD81, and reveal palmitoylation on the N- and C-terminal tails as well as the intracellular loop between transmembrane domains 2 and 3. One of these mutants lacks all five of its intracellular cysteines and therefore cannot be palmitoylated. This unpalmitoylated version of CD81 shows constitutive association with 14-3-3. Interestingly, we find that under oxidative conditions, CD81 palmitoylation is inhibited and that condition correlates with the association of CD81 and 14-3-3. These finding suggest that CD81 signaling events could be mediated by 14-3-3 adapter proteins, and these signals may be dependent on cellular redox.

14-3-3 Proteins↗

Signal transduction through nuclear factor kappa B in ischemia-reperfusion and heart failure.

Ischemic heart disease is the major cause of morbity and mortality in the Western world, with chronic heart failure as one complication. Ischemia-reperfusion injury may induce cardiomyocyte cell death by necrosis or apoptosis. The heart can be adapted to tolerate an ischemic event by preceeding brief episodes of ischemia and reperfusion, called preconditioning. Innate immunity has the latest years surfaced as important for the development of cardiovascular pathology as well as for myocardial protection. Nuclear factor kappa B (NFkappaB) is a redox sensitive transcription factor which contributes to the regulation of innate and adaptive immunity. NFkappaB regulates a battery of inflammatory genes, and has been indicated to play a role in the development of numerous pathological states. Activation of NFkappaB induces gene programs leading to transcription of factors which promote inflammation, among them leukocyte adhesion molecules, cytokines such as tumor necrosis factor alpha, and chemokines, but may in some situations also promote tissue remodelling, the resolution of inflammation, and transcription of some few substances with possible antiinflammatory effects. The present paper reviews the basic regulation of NFkappaB, and the possible role of NFkappaB activation in ischemia-reperfusion injury, in adaptation to ischemia-reperfusion injury, and in chronic heart failure.

Heart Diseases↗

Hepatic metabolic adaptation to endurance exercise: temporal and sex differences by multiomics integration and validation.

BACKGROUND: Although endurance exercise benefits liver health, sex-specific adaptive trajectories remain unclear. This study mapped dynamic liver adaptation in males and females during prolonged training and identified underlying molecular programs. METHODS: Using publicly available time-resolved liver multi-omics data generated by the Molecular Transducers of Physical Activity Consortium (MoTrPAC), we established a computational pipeline for differential analysis of transcriptomic, proteomic, phosphoproteomic, and metabolomic data with FDR correction, followed by FGSEA pathway enrichment. Kinase activities were inferred through ortholog mapping and PhosphoSitePlus. Cross-omics co-expression networks were constructed using WGCNA and topological overlap to link omics features with physiological phenotypes. For experimental validation, liver tissues were collected from endurance-trained Sprague-Dawley rats, and key nodes were confirmed by Western blotting, qRT-PCR, and immunofluorescence/immunohistochemical staining. Public scRNA-seq data were further integrated to map multi-omics signals to single-cell resolution and assess functional changes in specific cell types. RESULTS: The hepatic response to exercise stress was stage-specific, shifting from early transcriptional activation to later proteomic and metabolic remodeling. Multi-omics integration revealed distinct sex-associated adaptive trajectories: males were more strongly associated with energy metabolism, redox-related programs, and amino acid/organic acid catabolism, whereas females showed prominent membrane lipid remodeling, proteostasis -related programs, and mitochondrial/ribosomal translational features. Single-cell analysis showed that tissue remodeling occurred without major lineage turnover, instead involving altered communication among pre-existing cell communities. Validation of PPP1R3G identified a protein-dominant exercise-responsive marker, supporting the contribution of post-transcriptional or protein-level regulation. CONCLUSIONS: Hepatic adaptation to endurance stress follows a cross-omics evolutionary pattern with sex-specific reprogramming of energy supply and homeostatic maintenance. This time-resolved framework clarifies how exercise improves liver function and supports sex-oriented metabolic interventions and therapeutic target discovery.

Animals↗

[Status of oxido-reduction processes in cattle tissues during transition to the postnatal developmental period].

As known there is the identification of respiratory-metabolic acidosis in new born calves during the adaptation to the postnatal period. It was shown that the activity of glycolysis and citrate cycle was increasing and played the important role in the energy production in this period. It is supposed that the activation of redox state in the tissues may be inadequate to the structural and functional adaptation in the calves in conditions of partial identification of neonatal acidosis.

Animals↗

Temporal proteomic analysis reveals a three-phase adaptation strategy in Phytophthora cinnamomi during salinity stress.

Phytophthora cinnamomi, a highly invasive hemibiotrophic oomycete, threatens global agriculture, forestry, and native ecosystems. Although drought and temperature effects on P. cinnamomi-host interactions are well studied, current knowledge of abiotic stress responses in P. cinnamomi remains largely centered on infection and phytopathology, with limited molecular insight into the pathogen's direct response to salinity independent of its host. To address this gap, we combined growth assays, time-resolved proteomics, and network analysis to define how P. cinnamomi responds and adapts to salinity exposure. Growth assays showed that NaCl-modified agar enhanced mycelial expansion in a concentration-dependent manner, with 100&#xa0;mM NaCl significantly increasing growth at 48, 72, and 96&#xa0;h compared with controls, while 50&#xa0;mM NaCl remained comparable to control conditions. Temporal proteomic analysis of 100&#xa0;mM NaCl treatment at 0, 1, 6, 12, and 24&#xa0;h post treatment revealed dynamic shifts in protein abundance. Early induction of ROS (Reactive Oxygen Species)-detoxifying enzymes, including glutathione S-transferases and peroxidases, was consistent with ROS-specific staining assays. Network analysis identified modules enriched for redox regulation, ATP generation, ion transport, and translational control, highlighting multi-layered adaptation to elevated NaCl levels. Notably, clusters of conserved hypothetical proteins were strongly upregulated, indicating unexplored stress tolerance components in Phytophthora species. Here, we propose that P. cinnamomi rapidly activates a three-phase strategy involving metabolism readjustments, redox defenses, and cellular structure alterations under salinity conditions. With increasing soil salinization due to climate change, our study provides first mechanistic insights into P. cinnamomi's adaptive plasticity and ecological resilience to abiotic stress. SIGNIFICANCE: This study represents the first temporal proteomic analysis of salinity stress adaptation in Phytophthora cinnamomi, revealing a sophisticated three-phase adaptation strategy. This research fundamentally advances our understanding of how this globally destructive plant pathogen, P. cinnamomi, maintains environmental resilience. Our findings reveal proteome remodelling as a mechanistic framework for understanding stress tolerance in oomycetes, a group of microorganisms responsible for some of the world's most destructive agricultural and forest diseases. Our results show proteins involved in emergency damage control through metabolic recalibration to sustained adaptation. These findings have relevance for predicting pathogen behavior under climate change scenarios, where increasing soil salinity threatens agricultural productivity while simultaneously enhancing pathogen survival and virulence. Understanding how P. cinnamomi responds to prolonged salinity exposure may inform targeted biocontrol strategies and improve predictive models of disease pressure in salt-affected agricultural regions. The temporal analysis framework we present offers a broadly applicable approach for understanding microbial stress adaptation, with implications extending beyond plant pathology to environmental microbiology and biotechnology applications where stress tolerance is paramount.

Phytophthora↗

The mitochondrial type II peroxiredoxin F is essential for redox homeostasis and root growth of Arabidopsis thaliana under stress.

Peroxiredoxins (Prx) have recently moved into the focus of plant and animal research in the context of development, adaptation, and disease, as they function both in antioxidant defense by reducing a broad range of toxic peroxides and in redox signaling relating to the adjustment of cell redox and antioxidant metabolism. At-PrxII F is one of six type II Prx identified in the genome of Arabidopsis thaliana and the only Prx that is targeted to the plant mitochondrion. Therefore, it might be assumed to have functions similar to the human 2-Cys Prx (PRDX3) and type II Prx (PRDX5) and yeast 1-Cys Prx that likewise have mitochondrial localizations. This paper presents a characterization of PrxII F at the level of subcellular distribution, activity, and reductive regeneration by mitochondrial thioredoxin and glutaredoxin. By employing tDNA insertion mutants of A. thaliana lacking expression of AtprxII F (KO-AtPrxII F), it is shown that under optimal environmental conditions the absence of PrxII F is almost fully compensated for, possibly by increases in activity of mitochondrial ascorbate peroxidase and glutathione-dependent peroxidase. However, a stronger inhibition of root growth in KO-AtPrxII F seedlings as compared with wild type is observed under stress conditions induced by CdCl2 as well as after administration of salicylhydroxamic acid, an inhibitor of cyanide-insensitive respiration. Simultaneously, major changes in the abundance of both nuclear and mitochondria-encoded transcripts were observed. These results assign a principal role to PrxII F in antioxidant defense and possibly redox signaling in plants cells.

Adenosine Triphosphate↗

Electrical wiring of Pseudomonas putida and Pseudomonas fluorescens with osmium redox polymers.

Two different flexible osmium redox polymers; poly(1-vinylimidazole)12-[Os-(4,4'-dimethyl-2,2'-di'pyridyl)2Cl2](2+/+) (osmium redox polymer I) and poly(vinylpyridine)-[Os-(N,N'-methylated-2,2'-biimidazole)3](2+/3+) (osmium redox polymer II) were investigated for their ability to efficiently "wire" Pseudomonas putida ATCC 126633 and Pseudomonas fluorescens (P. putida DSM 6521), which are well-known phenol degrading organisms, when entrapped onto cysteamine modified gold electrodes. The two Os-polymers differ in redox potential and the length of the side chains, where the Os(2+/3+)-functionalities are located. The bacterial cells were adapted to grow in the presence of phenol as the sole source of organic carbon. The performance of the redox polymers as mediators was investigated for making microbial sensors. The analytical characteristics of the microbial sensors were evaluated for determination of catechol, phenol and glucose as substrates in both batch analysis and flow analysis mode.

2,2'-Dipyridyl↗