Nitric Oxide Detoxification Research Articles

High NO and N2O accumulation during nitrite denitrification in lab-scale sequencing batch reactor: influencing factors and mechanism.

Nitrous oxide (N2O) accumulation in biological nitrogen removal has drawn much attention in recent years; however, nitric oxide (NO) accumulation in denitrification was rarely studied. In this study, NO and N2O accumulation during nitrite denitrification in a lab-scale sequencing batch reactor (SBR) were investigated. Results showed that low pH (< 7) and high influent loading (> 360:90) (COD:NO2--N) caused serious NO and N2O accumulation. The maximal NO accumulation of 4.96 mg L-1 was observed at influent loading of 720:180 and the maximal N2O accumulation of 46.29 mg L-1 was found at pH of 6. The NO accumulation was far higher than the values reported in previous studies. In addition, the high NO accumulation could completely inhibit the activities of reductases involved in denitrification. High NO and N2O accumulation were mainly caused by significant free nitrous acid (FNA) and NO inhibition at low pH and high influent loading. There were significant differences on NO and N2O accumulation at different carbon to nitrogen (COD/N). Low COD/N (≤ 4) could mitigate NO accumulation, but led to high N2O accumulation. It is speculated that NO accumulation is related to the rapid denitrification with accumulated electron in anaerobic stage at high COD/N. N2O accumulation is attributed to intense electron competition at low COD/N. High dissolved oxygen (DO) of 4.04 mg L-1 was detected during NO detoxification in this experiment, which is speculated to be partly caused by NO dismutation.

Diverse effects of nitric oxide reductase NorV on Aeromonas hydrophila virulence-associated traits under aerobic and anaerobic conditions

NorV has been known to be an anaerobic nitric oxide reductase associated with nitric oxide (NO) detoxification. Recently, we showed that the norV gene of Aeromonas hydrophila was highly upregulated after co-culturing with Tetrahymena thermophila. Here, we demonstrated that the transcription and expression levels of norV were upregulated in a dose-dependent manner after exposure to NO under aerobic and anaerobic conditions. To investigate the roles of norV in resisting predatory protists and virulence of A. hydrophila, we constructed the norV gene-deletion mutant (ΔnorV). Compared to the wild type, the ΔnorV mutant showed no significant difference in growth at various NO concentrations under aerobic conditions but significantly stronger NO-mediated growth inhibition under anaerobic conditions. The deletion of norV exhibited markedly decreased cytotoxicity, hemolytic and protease activities under aerobic and anaerobic conditions. Also, the hemolysin co-regulated protein (Hcp) in the ΔnorV mutant showed increased secretion under aerobic conditions but decreased secretion under anaerobic conditions as compared to the wild-type. Moreover, the inactivation of norV led to reduced resistance to predation by T. thermophila, decreased survival within macrophages and highly attenuated virulence in zebrafish. Our data indicate a diverse role for norV in the expression of A. hydrophila virulence-associated traits that is not completely dependent on its function as a nitric oxide reductase. This study provides insights into an unexplored area of NorV, which will contribute to our understanding of bacterial pathogenesis and the development of new control strategies for A. hydrophila infection.

Iron-Sulfur Cluster Repair Contributes to Yersinia pseudotuberculosis Survival within Deep Tissues.

To successfully colonize host tissues, bacteria must respond to and detoxify many different host-derived antimicrobial compounds, such as nitric oxide (NO). NO has direct antimicrobial activity through attack on iron-sulfur (Fe-S) cluster-containing proteins. NO detoxification plays an important role in promoting bacterial survival, but it remains unclear if repair of Fe-S clusters is also important for bacterial survival within host tissues. Here we show that the Fe-S cluster repair protein YtfE contributes to the survival of Yersinia pseudotuberculosis within the spleen following nitrosative stress. Y. pseudotuberculosis forms clustered centers of replicating bacteria within deep tissues, where peripheral bacteria express the NO-detoxifying gene hmp. ytfE expression also occurred specifically within peripheral cells at the edges of microcolonies. In the absence of ytfE, the area of microcolonies was significantly smaller than that of the wild type (WT), consistent with ytfE contributing to the survival of peripheral cells. The loss of ytfE did not alter the ability of cells to detoxify NO, which occurred within peripheral cells in both WT and ΔytfE microcolonies. In the absence of NO-detoxifying activity by hmp, NO diffused across ΔytfE microcolonies, and there was a significant decrease in the area of microcolonies lacking ytfE, indicating that ytfE also contributes to bacterial survival in the absence of NO detoxification. These results indicate a role for Fe-S cluster repair in the survival of Y. pseudotuberculosis within the spleen and suggest that extracellular bacteria may rely on this pathway for survival within host tissues.

Effect of starvation time on NO and N2O production during heterotrophic denitrification with nitrite and glucose shock loading

Abstract Nitric oxide (NO) and nitrous oxide (N2O) production during biological nitrogen removal has been widely studied, however, the mechanism of starvation time on NO and N2O accumulation has not yet been well characterized. Nitrite denitrification, as a significant source of NO and N2O production, has received increasing attention. Therefore, the goal of this study was to investigate the effect of starvation time on NO and N2O accumulation during nitrite denitrification. Results showed that starvation time have a significantly effect on NO accumulation. High NO accumulation may be mainly related to the imbalance of electron distribution caused by feast after famine. N2O accumulation under all starvation tests included two stages, namely the exogenous denitrification and the endogenous denitrification. The N2O accumulation is mainly attributed to electron competition, free nitrous acid (FNA) inhibition, and starvation time. In addition, results suggest that moderate starvation time promotes the NO and N2O accumulation, especially, the starvation time affects NO accumulation more significantly than that of N2O. Interestingly, high dissolved oxygen (DO) was detected during NO detoxification, which is partly related to NO dismutation. The microbial community analysis revealed that the predominant bacterial genera were Phycisphaera, Thauera, Comamonas, Bdellovibrio, and Castellaniella, which belong to denitrifiers.

Repurposing Glyburide as Antileishmanial Agent to Fight Against Leishmaniasis

Leishmaniasis is caused by a protozoan parasite, Leishmania. It is common in more than 98 countries throughout the world. Due to insufficient availability of antileishmanial chemotherapeutics, it is an urgent need to search for new molecules which have better efficacy, low toxicity and are available at low cost. There is a high rate of diabetic cases throughout the world that is why we planned to test the antileishmanial activity of glyburide, an effective sugar lowering drug used for the treatment of diabetes. In this study, glyburide showed a significant decrease in the parasite growth and survival in vitro in a dose-dependent manner. Anti-leishmanial activity of glyburide was checked by culturing Leishmania donovani promastigotes in the presence of glyburide in a dose and time dependent manner. Docking study against Leishmania donovani-Trypanothione synthetase (LdTrySyn) protein was performed using Autodock Vina tool. Growth reversibility assay shows that growth of treated parasite was not reversed when transferred to fresh culture media after 7 days. Moreover, docking studies show efficient interactions of glyburide with key residues in the catalytic site of Leishmania donovani- Trypanothione synthetase (LdTrySyn), a very important leishmanial enzyme involved in parasite's survival by detoxification of Nitric Oxide (NO) species, generated by the mammalian host as a defense molecule. Thus this study proves that the drug-repurposing is a beneficial strategy for identification of new and potent antileishmanial molecules. The results suggest that glyburide binds to LdTrySyn and inhibits its activity which further leads to the altered parasite morphology and inhibition of parasite growth. Glyburide may also be used in combination with other anti-leishmanial drugs to potentiate the response of the chemotherapy. Overall this study provides information about combination therapy as well as a single drug treatment for the infected patients suffering from diabetes. This study also provides raw information for further in vivo disease model studies to confirm the hypothesis.

Reactive nitrogen species induced catalases promote a novel nitrosative stress tolerance mechanism in Vibrio cholerae

Vibrio cholerae faces nitrosative stress during successful colonization in intestine. Very little information is available on the nitrosative stress protective mechanisms of V. cholerae. Reports show that NorR regulon control two genes hmpA and nnrS responsible for nitric oxide (NO) detoxification in V. cholerae. In the present study we first time report a novel role of V. cholerae catalases under nitrosative stress. Using zymogram analysis of catalase we showed that KatB and KatG activity were induced within 30 min in V. cholerae in the presence of sodium nitroprusside (SNP), a NO donor compound. Surprisingly, V. cholerae cell survival was found to be decreased under nitrosative stress if catalase activities were blocked by ATz, a catalase inhibitor. Flow cytometry study was conducted to detect reactive oxygen species (ROS) and reactive nitrogen species (RNS) using DHE and DHR123, fluorescent probes respectively. Short exposure of SNP to V. cholerae did not generate ROS but RNS was detectable within 30 min. Total glutathione content was increased in V. cholerae cells under nitrosative stress. Furthermore, Superoxide dismutase (SOD) and Glutathione reductase (GR) activities remained unchanged under nitrosative stress in V. cholerae indicated antioxidant role of NO which could produce peroxynitrite. To investigate the role of catalase induction under nitrosative stress in V. cholerae, we conducted peroxynitrite reductase assay using cell lysates. Interestingly, SNP treated V. cholerae cell lysates showed lowest DHR123 oxidation compared to the control set. The extent of DHR123 oxidation was more in V. cholerae cell lysate when catalases were blocked by ATz.

Investigating the role of nitric oxide in plant root colonisation by Streptomyces spp.

Streptomyces is a genus of soil dwelling actinomycetes that play an important role in plant health through association with plant roots. They provide an array of benefits to the plant host such as infectious disease prevention and plant growth promotion. We investigate the role of nitric oxide (NO), a ubiquitous signalling molecule used by plants and bacteria alike, in root colonisation by Streptomyces coelicolor. Plating studies were conducted for Arabidopsis thaliana and Triticum aestivum. Relative colonisation was determined by comparing selective recovery of marked mutant strains, alongside a marked control. The effect of increased endogenous NO was interrogated with a deletion mutant of nsrR-hmpA – genes responsible for NO detoxification in Streptomyces. Strains were also engineered to express recombinant NO synthase genes, to investigate the impact of NO production by the bacteria. We show that S. coelicolor ΔnsrR-hmpA is significantly more competent at colonising T. aestivum rhizosphere compared to the control (P&lt;0.005). Endosphere colonisation is sporadic for both mutant and control, this observation is supported by fCLSM imaging. Preliminary data indicates that the Streptomyces strains engineered to express NO synthase at high levels, colonise poorly. This suggests that NO is a dynamic and finely tuned signalling molecule. We are excited to present promising new evidence to support an as yet undescribed link between NO and plant root colonisation by Streptomyces coelicolor. Understanding the mechanisms that underpin this process is the first step in exploiting these interactions for agricultural technology.

A multifaceted small RNA modulates gene expression upon glucose limitation in Staphylococcus aureus.

Pathogenic bacteria must rapidly adapt to ever-changing environmental signals resulting in metabolism remodeling. The carbon catabolite repression, mediated by the catabolite control protein A (CcpA), is used to express genes involved in utilization and metabolism of the preferred carbon source. Here, we have identified RsaI as a CcpA-repressed small non-coding RNA that is inhibited by high glucose concentrations. When glucose is consumed, RsaI represses translation initiation of mRNAs encoding a permease of glucose uptake and the FN3K enzyme that protects proteins against damage caused by high glucose concentrations. RsaI also binds to the 3' untranslated region of icaR mRNA encoding the transcriptional repressor of exopolysaccharide production and to sRNAs induced by the uptake of glucose-6 phosphate or nitric oxide. Furthermore, RsaI expression is accompanied by a decreased transcription of genes involved in carbon catabolism pathway and an activation of genes involved in energy production, fermentation, and nitric oxide detoxification. This multifaceted RNA can be considered as a metabolic signature when glucose becomes scarce and growth is arrested.

Identification of Genes Regulated by the Antitermination Factor NasT during Denitrification in Bradyrhizobium diazoefficiens.

The soybean symbiont Bradyrhizobium diazoefficiens grows anaerobically in the presence of nitrate using the denitrification pathway, which involves the nap, nir, nor, and nos genes. We previously showed that NasT acts as a transcription antitermination regulator for nap and nos gene expression. In the present study, we investigated the targets of NasT in B. diazoefficiens during denitrifying growth by performing transcription profiling with RNA-seq and quantitative reverse-transcription PCR. Most of the genes with altered expression in the absence of NasT were related to nitrogen metabolism, specifically several systems for branched-chain amino acid transport. The present results suggest that the reduced expression of genes involved in nitrogen acquisition leads to the induction of alternative sets of genes with similar functions. The ΔnasT mutant of B. diazoefficiens grew better than the wild type under denitrifying conditions. However, this enhanced growth was completely abolished by an additional loss of the narK or bjgb genes, which encode cytoplasmic systems for nitrite and nitric oxide detoxification, respectively. Since the expression of narK and bjgb was increased in the ΔnasT mutant, the growth of the ΔnasT mutant may be promoted by increased detoxification activity.

Siroheme Is Essential for Assimilation of Nitrate and Sulfate as Well as Detoxification of Nitric Oxide but Dispensable for Murine Virulence of Aspergillus fumigatus.

The saprophytic mold Aspergillus fumigatus is the most common airborne fungal pathogen causing severe invasive fungal infections in immunocompromised patients. Siroheme is a heme-like prosthetic group used by plants and microorganisms for sulfate and nitrate assimilation but is absent in higher eukaryotes. Here, we investigated the role of siroheme in A. fumigatus by deletion of the gene encoding the bifunctional dehydrogenase/ferrochelatase enzyme Met8. Met8-deficiency resulted in the inability to utilize sulfate and nitrate as sulfur and nitrogen sources, respectively. These results match previous data demonstrating that siroheme is an essential cofactor for nitrite and sulfite reductases. Moreover, Met8-deficiency caused significantly decreased resistance against nitric oxide (NO) underlining the importance of nitrite reductase in NO detoxification. Met8-deficiency did not affect virulence in murine models for invasive aspergillosis indicating that neither NO-detoxification nor assimilation of sulfate and nitrate play major roles in virulence in this host. Interestingly, Met8-deficiency resulted in mild virulence attenuation in the Galleria mellonella infection model revealing differences in interaction of A. fumigatus with G. mellonella and mouse.

Loss of DksA leads to multi-faceted impairment of nitric oxide detoxification by Escherichia coli

Human immune cells use a battery of toxic chemicals to eliminate invading bacteria. One of those compounds is nitric oxide (NO) and pathogens have evolved various strategies to defend themselves against this immune effector. Enzymatic detoxification is a common approach used by many bacteria, and Escherichia coli employs several enzymes to deal with NO, such as Hmp a flavohemoprotein. In addition to nitrosative stress, nutrient deprivation has been found to play an important role in phagosomal antimicrobial activity. Interestingly, recent work in Salmonella has suggested that DksA, a transcription regulator associated with the stringent response, is a molecular node for integration of nutritional and nitrosative stress signals. Here, we found that, in E. coli, loss of DksA profoundly impairs aerobic NO detoxification, approaching the detoxification capacity of Δhmp, which exhibits little-to-no NO detoxification within aerobic conditions. Investigation of this phenotype revealed that under NO stress ΔdksA suffered from low hmp transcript levels, considerably impaired protein output from the hmp promoter, and reduced catalysis by Hmp when present. These data demonstrate that DksA is critical for NO detoxification by E. coli and that loss of this regulator leads to NO defense deficiencies that span multiple levels.

Phylogenomics Reveal the Dynamic Evolution of Fungal Nitric Oxide Reductases and Their Relationship to Secondary Metabolism.

Fungi expressing P450nor, an unconventional nitric oxide (NO) reducing cytochrome P450, are considered significant contributors to environmental nitrous oxide (N2O) emissions. Despite extensive efforts, fungal contributions to N2O emissions remain uncertain. For example, the majority of N2O emitted from antibiotic-amended soil microcosms is attributed to fungal activity, yet axenic fungal cultures do not couple N-oxyanion respiration to growth and these fungi produce only minor quantities of N2O. To assist in reconciling these conflicting observations and produce a benchmark genomic analysis of fungal denitrifiers, genes underlying denitrification were examined in >700 fungal genomes. Of 167 p450nor—containing genomes identified, 0, 30, and 48 also harbored the denitrification genes narG, napA, or nirK, respectively. Compared with napA and nirK, p450nor was twice as abundant and exhibited 2–5-fold more gene duplications, losses, and transfers, indicating a disconnect between p450nor presence and denitrification potential. Furthermore, cooccurrence of p450nor with genes encoding NO-detoxifying flavohemoglobins (Spearman r = 0.87, p = 1.6e−10) confounds hypotheses regarding P450nor’s primary role in NO detoxification. Instead, ancestral state reconstruction united P450nor with actinobacterial cytochrome P450s (CYP105) involved in secondary metabolism (SM) and 19 (11%) p450nor-containing genomic regions were predicted to be SM clusters. Another 40 (24%) genomes harbored genes nearby p450nor predicted to encode hallmark SM functions, providing additional contextual evidence linking p450nor to SM. These findings underscore the potential physiological implications of widespread p450nor gene transfer, support the undiscovered affiliation of p450nor with fungal SM, and challenge the hypothesis of p450nor’s primary role in denitrification.

Synthesis and detoxification of nitric oxide in the plant beneficial rhizobacterium Bacillus amyloliquefaciens SQR9 and its effect on biofilm formation

Nitric oxide (NO) is an important gas signal that regulates many biological processes, and due to the high nitrogen recycling activity in the rhizosphere, NO is an important signaling molecule in this region. Thus, an understanding of the effect of NO on the rhizomicrobiome, especially on plant beneficial rhizobacteria, is important for the use of these bacteria in agriculture. In this study, the effect of exogenous NO on the beneficial rhizobacterium Bacillus amyloliquefaciens SQR9 was investigated. The results showed that low concentrations of NO increased the ability of the strain SQR9 to form biofilms, while high concentrations of NO inhibited the growth of this bacterium. The SQR9 gene yflM encodes nitric oxide synthase (NOS), which is used to synthesize NO, while the gene ykvO encodes a sepiapterin reductase that is used to synthesize tetrahydrobiopterin, the coenzyme of NOS. Isothermal titration calorimetry and high-performance liquid chromatography analyses demonstrated an interaction between YkvO and NADPH. SQR9 has two hmp genes, although only one was observed to be responsible for NO detoxification through oxidization. This study revealed the effect of NO on plant beneficial rhizobacterium and assessed the ability of this strain to adapt to exogenous NO, which will help to improve the application of this strain in agricultural production.

Detoxification of NO and CO gases over effectively substituted Pd and Rh in cupric oxide catalysts

Precious metals like Pd and Rh mixed with metal oxides exhibit a superior CO adsorption capacity, and thus their substitution has considerable effect on surface property of cupric oxide. This communication focuses on Pd and Rh substitution in cupric oxide and their catalytic application in detoxification of both nitric oxide (NO) and carbon monoxide (CO) gases by redox reaction. The synthesised catalysts were characterised by X-ray diffraction, X-ray photoelectron spectroscopy, transmission electron microscopy and Brunauer–Emmett–Teller. In our study, we discovered that when doped with not more than 5% concentration of Pd and Rh the catalytic activity of cupric oxide was found to be increased. These electron-rich metals have a promotional effect on the catalytic activity for detoxification reactions. Effect of partial pressures of O2 and CO on the CO–O2 and NO–CO redox reactions was studied. Chemisorption of CO and NO was investigated using pulse titrations. Pd-doped CuO gave good catalytic reaction and showed better reaction stability in the presence and absence of the moisture.

Type II flavohemoglobin of Mycobacterium smegmatis oxidizes d-lactate and mediate electron transfer

Two distantly related flavohemoglobins (FHbs), MsFHbI and MsFHbII, having crucial differences in their heme and reductase domains, co-exist in Mycobacterium smegmatis. Function of MsFHbI is associated with nitric-oxide detoxification but physiological relevance of MsFHbII remains unknown. This study unravels some unique spectral and functional characteristics of MsFHbII. Unlike conventional type I FHbs, MsFHbII lacks nitric-oxide dioxygenase and NADH oxidase activities but utilizes d-lactate as an electron donor to mediate electron transfer. MsFHbII carries a d-lactate dehydrogenase type FAD binding motif in its reductase domain and oxidizes d-lactate in a FAD dependent manner to reduce the heme iron, suggesting that the globin is acting as an electron acceptor. Importantly, expression of MsFHbII in Escherichia coli imparted protection under oxidative stress, suggesting its important role in stress management of its host. Since M. smegmatis lacks the gene encoding for d-lactate dehydrogenase and d-lactate is produced during aerobic metabolism and also as a by-product of lipid peroxidation, the ability of MsFHbII to metabolize d-lactate may provide it a unique ability to balance the oxidative stress generated due to accumulation of d-lactate in the cell and at the same time sequester electrons and pass it to the respiratory apparatus.

Nitric Oxide Signalling in Yeast.

Nitric oxide (NO) is a cellular signalling molecule widely conserved among organisms, including microorganisms such as bacteria, yeasts, and fungi, and higher eukaryotes such as plants and mammals. NO is mainly produced by the activities of NO synthase (NOS) or nitrite reductase (NIR). There are several NO detoxification systems, including NO dioxygenase (NOD) and S-nitrosoglutathione reductase (GSNOR). NO homeostasis, based on the balance between NO synthesis and degradation, is important for regulating its physiological functions, since an excess of NO causes nitrosative stress due to the high reactivity of NO and NO-derived compounds. In yeast, NO may be involved in stress responses, but the role of NO and the mechanism underlying NO signalling are poorly understood due to the lack of mammalian NOS orthologs in the yeast genome. NOS and NIR activities have been observed in yeast cells, but the gene-encoding NOS and the mechanism by which NO production is catalysed by NIR remain unclear. On the other hand, yeast cells employ NOD and GSNOR to maintain intracellular redox balance following endogenous NO production, treatment with exogenous NO, or exposure to environmental stresses. This article reviews NO metabolism (synthesis, degradation) and its regulation in yeast. The physiological roles of NO in yeast, including the oxidative stress response, are also discussed. Such investigations into NO signalling are essential for understanding how NO modulates the genetics and physiology of yeast. In addition to being responsible for the pathology and pharmacology of various degenerative diseases, NO signalling may be a potential target for the construction and engineering of industrial yeast strains.

Nitric oxide signaling in yeast.

As a cellular signaling molecule, nitric oxide (NO) is widely conserved from microorganisms, such as bacteria, yeasts, and fungi, to higher eukaryotes including plants and mammals. NO is mainly produced by NO synthase (NOS) or nitrite reductase (NIR) activity. There are several NO detoxification systems, including NO dioxygenase (NOD) and S-nitrosoglutathione reductase (GSNOR). NO homeostasis based on the balance between NO synthesis and degradation is important for the regulation of its physiological functions because an excess level of NO causes nitrosative stress due to the high reactivity of NO and NO-derived compounds. In yeast, NO may be involved in stress responses, but NO and its signaling have been poorly understood due to the lack of mammalian NOS orthologs in the genome. Even though the activities of NOS and NIR have been observed in yeast cells, the gene encoding NOS and the NO production mechanism catalyzed by NIR remain unclear. On the other hand, yeast cells employ NOD and GSNOR to maintain an intracellular redox balance following endogenous NO production, exogenous NO treatment, or environmental stresses. This article reviews NO metabolism (synthesis, degradation) and its regulation in yeast. The physiological roles of NO in yeast, including the oxidative stress response, are also discussed here. Such investigations into NO signaling are essential for understanding the NO-dependent genetic and physiological modulations. In addition to being responsible for the pathology and pharmacology of various degenerative diseases, NO signaling may be a potential target for the construction and engineering of industrial yeast strains.

Structure of Escherichia coli Flavodiiron Nitric Oxide Reductase

Flavodiiron proteins (FDPs) are present in organisms from all domains of life and have been described so far to be involved in the detoxification of oxygen or nitric oxide (NO), acting as O2 and/or NO reductases. The Escherichia coli FDP, named flavorubredoxin (FlRd), is the most extensively studied FDP. Biochemical and in vivo studies revealed that FlRd is involved in NO detoxification as part of the bacterial defense mechanisms against reactive nitrogen species. E. coli FlRd has a clear preference for NO as a substrate in vitro, exhibiting a very low reactivity toward O2. To contribute to the understanding of the structural features defining this substrate selectivity, we determined the crystallographic structure of E. coli FlRd, both in the isolated and reduced states. The overall tetrameric structure revealed a highly conserved flavodiiron core domain, with a metallo-β-lactamase-like domain containing a diiron center, and a flavodoxin domain with a flavin mononucleotide cofactor. The metal center in the oxidized state has a μ-hydroxo bridge coordinating the two irons, while in the reduced state, this moiety is not detected. Since only the flavodiiron domain was observed in these crystal structures, the structure of the rubredoxin domain was determined by NMR. Tunnels for the substrates were identified, and through molecular dynamics simulations, no differences for O2 or NO permeation were found. The present data represent the first structure for a NO-selective FDP.

Catalytic activity and mechanistic approach of NO reduction by CO over M0.05Co2.95O4 (M = Rh, Pd & Ru) spinel system

Pd, Rh and Ru doped cobalt oxide spinels have been prepared by citric acid assisted sol-gel method to yield nano-catalysts. Compositions have been characterized by XRD, FTIR, TG/DTA, BET, SEM, TEM, TPD and XPS techniques. Simultaneous catalytic detoxification of nitric oxide and carbon monoxide is investigated over the doped and pristine catalysts. Metal doping is found to enhance the activity of the catalysts due to their better adsorption capacity. Moisture and oxygen tolerance is investigated for Rh and Pd substituted catalysts. A probable reaction mechanism on the catalyst surface has been proposed.

Evaluation of globins expression in brain, heart, and lung in rats exposed to side stream cigarette smoke.

The side stream cigarette smoke (SSCS) is a contributing factor in the pathogenesis of cigarette smoking-induced toxicity. Hemoglobin (Hb), myoglobin (Mb), neuroglobin (Ngb), and cytoglobin (Cygb) are globins with different distributions and functions in the tissues and have similar actions by providing O2 (oxygen) for respiratory chain, detoxification of ROS and nitric oxide (NO), and protect tissues against irreversible lesions. We aimed to investigate the effects of SSCS exposure on gene and protein expression of Ngb, Cygb, and Mb in different tissue. The Ngb and Cygb gene and protein expression in the cerebral cortex increased after 1 week of rat exposure to SSCS. In hippocampus, the Ngb gene and protein expression increased after 1 week or more of exposure and no change was observed in Cygb gene and protein expression. In myocardium, Mb and Cygb gene expression increased at 1 and 4 weeks of exposure, while protein expression of both increased at 1, 2, 3, and 4 weeks. In lung, observed an increase in Cygb gene and protein expression after 2, 3, and 4 weeks of exposure. The findings suggest that SSCS modulates Ngb, Cygb, and Mb in central and peripheral tissue © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1252-1261, 2017.