Role Of Carbon Monoxide Research Articles

‘That which does not kill us only makes us stronger’: the role of carbon monoxide in thermophilic microbial consortia

Carbon monoxide (CO), while a potent toxin, is also a key intermediate in major autotrophic pathways such as methanogenesis and acetogenesis. The ability of purple sulfur bacteria to use CO as an energy source was first described by Uffen in 1976. The prototype extremely thermophilic carboxydotroph Carboxydothermus hydrogenoformans was described in 1991. Eight bacteria and one archaeon that utilize CO have since been isolated and described from diverse geothermal environments. They derive energy from the oxidation of CO with water to form CO(2) and H(2). Most of these isolates thrive with headspace CO partial pressures around 1 atm, which is grossly elevated relative to CO concentrations in geothermal effluents. To account for this, we suggest that under consortial growth conditions the carboxydotrophs occupy microniches in which biogenic CO accumulates locally to high concentrations. CO oxidizers dissipate these potentially toxic CO hot spots with the production of H(2), CO(2) and acetate whose subsequent oxidation fuels other thermophiles. The identification of genes related to anaerobic CO oxidation in many metagenomic databases attests to widespread distribution of carboxydotrophs. Current evidence suggests that CO-oxidizing bacteria and archaea hold a vital niche in thermophilic ecosystems.

Possible contribution of endogenous carbon monoxide to the development of allergic rhinitis in guinea pigs

BackgroundThe mechanisms responsible for the development of allergic rhinitis(AR) are not fully understood. The present study was designed to explore the possible roles of carbon monoxide(CO) on the pathogenesis of AR.MethodsAR guinea pig model was established by nasal ovalbumin sensitization. Twenty-four AR guinea pigs were divided into four groups, 6 in each: Saline control group, AR sensitized group, Hemin treated group, and Zinc protoporphyrin (ZnPP) treated group. The frequency of sneezing and nose rubbing was recorded. Leukocyte infiltration in nasal lavage fluid, serum IgE level and plasma CO were measured. Expression of heme oxygenase-1 (HO-1) mRNA in nasal mucosa was determined by real time RT-PCR, and expression of HO-1 protein was detected by immunohistochemistry.ResultsThe frequency of sneezing and nose rubbing, leukocyte infiltration, serum IgE, plasma CO, and HO-1 mRNA levels in sensitized guinea pigs were higher than those of control (P < 0.05). Except for serum IgE level, all above parameters were even higher (P < 0.05) when treated with Hemin, a heme oxygenase-1 inducer; but significantly decreased (P < 0.05) when treated with ZnPP, a heme oxygenase inhibitor. Immunohistochemical results showed that positive staining of HO-1 was present in the lamina of mucosa of sensitized guinea pigs, and there was an increase of HO-1 immunoreactivity with Hemin administration (P < 0.05) and a decrease with ZnPP treatment.ConclusionThe endogenous CO may take part in the inflammation process of AR and is positively correlated with expression of HO-1 in nasal mucosa. Endogenous CO plays a significant role in the pathogenesis of AR.

Role of Carbon Monoxide in Blood Pressure Regulation

Carbon monoxide (CO) is an odorless, colorless, tasteless gas that is generated in the environment as the result of combustion from stoves and engines among other sources. Approximately 500 people per year in the United States are victims of nonfire-associated CO poisoning according to the Centers for Disease Control and Prevention. CO poisoning is often fatal because of its interaction with hemoglobin, which renders it incapable of carrying oxygen-causing organs to become severely hypoxic. CO inhalation is believed to be fatally toxic at concentrations as little as 800 parts per million (ppm) or 0.08% in the air. Despite the lethal nature of this gas, several recent studies suggest that CO inhalation at low doses (≤250 ppm), as well as increases in CO levels using CO releasing molecules (CORMs), offers protection against ischemic injury in the heart, liver, and kidney.1–4 CO is endogenously produced in the body as a result of the metabolism of heme by heme oxygenase (HO), as well as from lipid peroxidation.5,6 The catabolism of heme by HO also produces an equimolar amount of biliverdin, which is rapidly converted in the cell to bilirubin by the enzyme biliverdin reductase.7 There are 2 major isoforms of HO responsible for CO production. HO-1 is expressed at very low levels under normal conditions but is highly induced by several stimuli, including heavy metals, ultraviolet light, endotoxin, shear stress, hypoxia, and oxidants.8 HO-2 is the constitutively expressed form of the enzyme with the highest levels observed in the brain and testes.9 Experimental evidence has demonstrated that systemic induction of HO has several beneficial actions on the cardiovascular system, including lowering of blood pressure, protection against myocardial infarction, and prevention of atherosclerosis.10–12 Although the cardiovascular actions of HO induction have been established, the role of CO in …

Interdiction of the Diabetic State in NOD Mice by Sustained Induction of Heme Oxygenase: Possible Role of Carbon Monoxide and Bilirubin

The aims of the present study were to assess whether sustained HO-1 expression could moderate or prevent diabetes in an animal model of the disease and, if so, to examine the possible mechanisms involved. Our results showed that HO-1 expression and HO activity were upregulated in the pancreas of non-obese diabetic (NOD) mice by the weekly administration of cobalt protoporphyrin (CoPP). Blood glucose levels in CoPPtreated mice decreased to normal, but continuously increased in untreated controls. Beta-cell numbers were preserved in the islets of CoPP-treated mice, whereas no beta cells were found in untreated diabetic mice. The number of CD11c(+) dendritic cells was significantly decreased in the pancreas of CoPP-treated NOD mice, but this effect was reversed by the inhibition of HO activity. Increased levels of HO-1 produced a new pancreatic phenotype, as reflected by increases in phosphorylated AKT, BcL-xL and RSK levels, and decreases in O(2)- and 3-NT levels. These novel findings provide a link between the increase in HO-1 activity, with its concurrent enhanced production of carbon monoxide (CO) and bilirubin, a decrease in infiltrated CD11c(+) dendritic cells and an increase in anti-apoptotic proteins, including RSK and BcL-xL, in the interdiction of the diabetic state.

The protective role of carbon monoxide in ventilator induced lung injury

The protective role of carbon monoxide in ventilator induced lung injury

Role of carbon monoxide in electrically induced non-adrenergic, non-cholinergic relaxations in the guinea-pig isolated whole trachea.

Nitric oxide (NO) and vasoactive intestinal peptide (VIP) are considered transmitters of non-adrenergic, non-cholinergic (NANC) relaxations in guinea-pig trachea, whereas the role of carbon monoxide (CO) is unknown. This study was designed to assess the participation of CO, and to investigate the localization of haem oxygenase-2 (HO-2), the CO-producing enzyme, in tracheal neurons. NANC responses to electrical field stimulation (EFS) at 3 and 10 Hz were evaluated in epithelium-free whole tracheal segments as intraluminal pressure changes. Drugs used were: L-nitroarginine methyl ester (L-NAME, 100 microM) to inhibit NO synthase (NOS), alpha-chymotrypsin (2 U ml(-1)) to inactivate VIP, zinc protoporphyrin-IX (ZnPP-IX, 10 microM) to inhibit HO-2, and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 microM), a soluble guanylyl cyclase inhibitor. For immunohistochemistry, tissues were exposed to antibodies to PGP 9.5, a general neuronal marker, HO-2 and NOS, and processed with an indirect immunofluorescence method. alpha-Chymotrypsin did not affect NANC relaxations. ODQ inhibited NANC responses by about 60%, a value similar to that obtained by combining L-NAME and ZnPP-IX. The combination of ODQ, L-NAME and ZnPP-IX reduced the responses by 90%. Subpopulations of HO-2 positive neurons containing NOS were detected in tracheal sections. In the guinea-pig trachea, NANC inhibitory responses at 3 and 10 Hz use NO and CO as main transmitters. Their participation is revealed following inhibition of NOS, HO-2 and soluble guanylyl cyclase. The involvement of CO as a relaxing transmitter paves the way for novel therapeutic approaches in the treatment of airway obstruction.

The Roles of Carbon Monoxide in Islets

Table 1. Summary of heme oxygenase (HO) isoforms HO-1 HO-2 HO-3 HO-2 amino acid homology ~40% 100% ~90% Physiological roles Heme catabolism Anti-oxidant defense Modulation of vascular tone & liver perfusion Neural signaling Anti-inflammatory actions Down-modulation of Adhesion molecule expression Regulation of hemo-proteins activity Heme catabolism Heme binding Maintenance of vascular tone Neural signaling Heme binding Regulation of heme dependent genes

Role of carbon monoxide in cardiovascular function

Role of carbon monoxide in cardiovascular function

Mechanisms of Heme Oxygenase-1-Mediated Cardiac and Pulmonary Vascular Protection in Chronic Hypoxia: Roles of Carbon Monoxide and Bilirubin

Mechanisms of Heme Oxygenase-1-Mediated Cardiac and Pulmonary Vascular Protection in Chronic Hypoxia: Roles of Carbon Monoxide and Bilirubin

Carbon monoxide, but not endothelin-1, plays a major role for the hepatic microcirculation in a murine model of early systemic inflammation

Endothelin-1 and carbon monoxide play a major role in the regulation of liver microcirculation in numerous disease states. During sepsis and endotoxemia, elevated formation of endothelin-1 results in reduced sinusoidal blood flow. However, the role of carbon monoxide and endothelin-1 and its receptors endothelin receptor A and endothelin receptor B in the deranged liver microcirculation during early systemic inflammation remains unclear. Prospective, randomized, controlled experiment. University animal laboratory. Male C57/BL6 mice, weighing 23-27 g. To induce a systemic inflammation, mice were treated with 1 hr of bilateral hind limb ischemia followed by 3 hrs or 6 hrs of reperfusion. Animals were randomly exposed to the nonselective endothelin receptor antagonist Ro-61-6612 (Tezosentan) and/or a continuous endothelin-1 infusion. Different animals were randomized to methylene chloride gavage or carbon monoxide inhalation during the reperfusion period. After ischemia/reperfusion, endothelin-1 plasma concentrations, endothelin-1 messenger RNA expression, and endothelin receptor A and B messenger RNA expression revealed no significant changes when compared with sham animals. After 6 hrs of ischemia/reperfusion, hepatic microcirculatory variables (sinusoidal density, sinusoidal diameter, and red blood cell velocity) deteriorated. Tezosentan after 6 hrs of ischemia/reperfusion did not improve the liver microcirculation, whereas the continuous infusion of endothelin-1 after 6 hrs of ischemia/reperfusion further impaired sinusoidal blood flow. Tezosentan treatment did not produce any alterations in hepatocellular injury or hepatic redox status when compared with the untreated animals receiving 6 hrs of ischemia/reperfusion. Animals receiving 6 hrs of ischemia/reperfusion and exposed to methylene chloride gavage or inhaled carbon monoxide during limb reperfusion showed significantly improved microcirculatory variables, hepatic redox status, and attenuated hepatocellular injury. These data suggest that endothelin-1 and the endothelin receptors A and B are not responsible for the observed hepatic microcirculatory and cellular dysfunction during early systemic inflammation, but exposure to exogenous carbon monoxide protected the hepatic microcirculation and improved the impaired hepatic cellular integrity and the hepatocellular redox status.

The role of carbon monoxide and nitric oxide in hyperosmolality-induced atrial natriuretic peptide release by hypothalamus in vitro

We evaluated the participation of the nitrergic and carbon monoxide (CO) systems in the atrial natriuretic peptide (ANP) release induced by osmotic stimulation of the rat anterior and medial basal hypothalamus (BH) fragments in vitro. The increase in the medium osmolality (NaCl, 340 mOsm/kg H 2O) induced an elevated ANP release, which was associated with a decrease in nitric oxide synthase (NOS) activity ( p<0.001), nitric oxide (NO) production and nitrate ( p<0.001) release into the medium. The NO donors sodium nitroprusside (SNP, 300 μM), S-nitroso- N-acetylpenicillamine (SNAP, 300 μM) and 3-morpholinylsydnoneimine chloride (SIN-1, 300 μM) promoted a significant decrease in ANP release in response to hyperosmolality ( p<0.001). ANP release observed in the present study did not result from injury to the BH caused by the increase in medium osmolality nor a toxic effect of the NO donors as demonstrated by the ANP release after incubation with KCl (56 mM). Furthermore, hyperosmolality or NO donors did not increase the LDH content in the medium. The hyperosmotic-induced ANP release and reduction of NOS activity were prevented by the heme oxygenase inhibitor, zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG). In conclusion, these results suggest that NO, the production of which is dependent on CO, modulates the osmolality-induced ANP release by BH fragments.

The role of carbon monoxide in the gastrointestinal tract.

Carbon monoxide (CO) is a biologically active product of haem metabolism that contributes to the normal physiology of the gastrointestinal tract. In this article, we review recent data showing that CO is an integral regulator of gastrointestinal motility and an important factor in the response to gastrointestinal injury. CO is generated by haem oxygenase-2 (HO-2), which is constitutively expressed in many inhibitory neurones of the vertebrate enteric nervous system. The membrane potential gradients along and across the muscle layers of the gastrointestinal tract require the generation of CO by haem oxygenase-2. The presence of CO is also necessary for normal inhibitory neurotransmission in circular smooth muscle and appears to permit nitric oxide-mediated inhibitory neurotransmission. Genetic deletion of the haem oxygenase-2 gene in mice slows gut transit. The other major CO synthetic enzyme, haem oxygenase-1 (HO-1) is induced under conditions of stress or injury. Recent studies have demonstrated that up-regulation of haem oxygenase-1 protects the gut from several types of gastrointestinal injury, suggesting that CO or induction of HO-1 may find therapeutic use in gastrointestinal diseases and injuries. Furthermore, it is anticipated that the understanding of CO-mediated signalling in the gastrointestinal tract will inform studies in other tissues that express haem oxygenases.

Oxygen and carbon monoxide role on the electrical response of a non-Nernstian potentiometric gas sensor; proposition of a model

The sensor used for the study was obtained from a solid electrolyte fitted with two metal electrodes (gold and platinum, respectively) located in the same gas mixture and was made using the screen printing technology. A kinetic model able to account for the electrical responses obtained in the presence of oxygen and carbon monoxide is proposed. This model is mainly based on the existence of several oxygen species adsorbed on the surface of the device and on the ideally polarizable properties of the electrodes. Action of carbon monoxide is assumed to occur according to a Langmuir–Hinshelwood model, which involves the consumption of oxygen species considered as a weakly metal-bonded particle. The simulations reveal that such a model is able to account for the complex influence of carbon monoxide, the oxygen pressure and the temperature on the electrical sensor’s response.

Development of the utero-placental circulation: the role of carbon monoxide and nitric oxide in trophoblast invasion and spiral artery transformation.

It is now well known that in order to establish human hemochorial placentation and to provide a progressive increase in blood supply to the growing fetus, the uterine spiral arteries must undergo considerable alterations. This physiological modification is thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Despite intensive research our understanding of the mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are sill poorly understood. This is partly due to difficulties in obtaining "true" placental bed biopsies and most investigators have relied on in vitro models of trophoblast invasion. This article describes the morphological changes that occur within the placental bed throughout human pregnancy along with a review of the various studies which have attempted to sample the placental bed. Thereafter, follows a review of the evidence that invasive trophoblast can release the vasoactive agents nitric oxide and/or carbon monoxide which, in turn, could contribute to early physiological changes in spiral arteries prior to destruction of the smooth muscle within the vessel wall. Current evidence supports the idea that trophoblast-derived carbon monoxide may contribute to spiral artery modification. In contrast there is no evidence for a similar role by nitric oxide.

Antioxidant compounds EGB-761 and BN-52021 attenuate brain edema formation and hemeoxygenase expression following hyperthermic brain injury in the rat.

Role of carbon monoxide (CO) in hyperthermic brain injury induced brain pathology was examined in a rat model using immunohistochemistry of the hemeoxygenase-2 (HO-2) enzyme. Exposure of rats to 4 h heat stress at 38 degrees C resulted in profound hyperthermia, breakdown of the blood-brain barrier (BBB), brain edema formation, cell damage and expression of HO-2 in several brain regions. Pretreatment with potent antioxidant compounds EGB-761 and BN-52021 markedly reduced the HO-2 expression, BBB breakdown, brain edema formation and cell damage without attenuating the hyperthermic response. This effect was most marked in animals treated with EGB-761. These observations suggest that upregulation of HO-2 representing generation of CO plays important roles in hyperthermic brain injury, and oxidative stress seems to be one of the most important signals in inducing HO-2 expression in hyperthermia, not reported earlier.

Role of carbon monoxide in glutamate receptor-induced dilation of newborn pig pial arterioles.

The hypothesis that glutamate dilates pial arterioles of newborn pigs through the production of carbon monoxide (CO) was addressed. Anesthesized newborn pigs were equipped with cranial windows to measure pial arteriolar responses to stimuli. Heme oxygenase (HO) inhibitors added topically inhibited dilation to glutamate and to specific glutamate receptor agonists. The initial dilation to glutamate (10(-5) M) was 22% from baseline without an inhibitor and decreased to 9% with the HO inhibitor chromium mesoporphyrin (CrMP). Inhibition of dilation upon HO inhibition was similar when specific glutamate receptor agonists were employed. RS-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid caused 24% dilation from the baseline without an inhibitor, and the dilation was decreased to 1% with tin protoporphyrin (SnPP). (RS)-2-amino-3-(3-hydroxy-5-t-butylisoxazol-4-yl)propionic acid (kainate receptors) caused dilation of 18% from baseline without an inhibitor, but only 2% when tin mesoporphyrin was applied. 1-Aminocyclopropanecarboxylic acid (N-methyl-D-aspartate receptors) dilated pial arterioles 33% from baseline in control, but only to 2% in the presence of SnPP. Neither copper mesoporphyrin, which does not inhibit HO, nor light-inactivated CrMP affected the dilations. Furthermore, cerebral microvessels removed from the brain produced CO (stable isotope dilution gas chromatography-mass spectrometry), and this production was dose dependently increased by glutamate and inhibited by metal porphyrin HO inhibitors. These data suggest that dilation of newborn pig pial arterioles to glutamate and specific glutamate receptor agonists involves vascular production of CO. Additional cerebral sources of CO also could be stimulated by glutamate and contribute to the dilation.

Marked Role of Carbon Monoxide in the Formation of Benzene During CH4-CO Reaction Over Rh/SiO2 Catalysts

Temperature-programmed desorption (He-TPD) and temperature-programmed reaction with hydrogen (H2-TPR), carbon monoxide (CO-TPR) or methane (CH4-TPR) were carried out to elucidate the benzene formation mechanism as well as the role of CO during CH4-CO reaction over SiO2-supported Rh catalysts. The steady-state surface for the CH4-CO reaction was different from that of the CH4 decomposition reaction. The existence of benzene-like adsorbed species as “building blocks” was demonstrated on the CH4-CO reaction surface, while no such higher hydrocarbon adsorbed species was detected in the case of the CH4 decomposition surface. On the contrary, in CO-TPR experiments various unsaturated hydrocarbons were released from the steady-state CH4 decomposition surface, which was not the case from the CH4-CO reaction surface. It is concluded that adsorbed CO may play an important role to enhance the C-C bond formation of carbonaceous species, which correlates deeply with the novel phenomenon of selective benzene formation in the CH4-CO reaction.

ChemInform Abstract: Novel Role of Carbon Monoxide as a Lewis Acid Catalyst for Friedel—Crafts Reaction.

AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

Novel role of carbon monoxide as a Lewis acid catalyst for Friedel-Crafts reaction.

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTADDITION / CORRECTIONThis article has been corrected. View the notice.Novel Role of Carbon Monoxide as a Lewis Acid Catalyst for Friedel−Crafts ReactionSensuke Ogoshi, Hiromitsu Nakashima, Kazumasa Shimonaka, and Hideo KurosawaView Author Information Department of Applied Chemistry Faculty of Engineering, Osaka University Suita, Osaka 565, Japan Cite this: J. Am. Chem. Soc. 2001, 123, 35, 8626–8627Publication Date (Web):August 8, 2001Publication History Received27 June 2001Revised18 July 2001Published online8 August 2001Published inissue 1 September 2001https://doi.org/10.1021/ja0165032Copyright © 2001 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views935Altmetric-Citations22LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit Read OnlinePDF (27 KB) Get e-AlertsSUBJECTS:Aromatic compounds,Hydrocarbons,Inorganic carbon compounds,Lewis acids,Oxides Get e-Alerts

Roles of carbon monoxide in leukocyte and platelet dynamics in rat mesenteric during sevoflurane anesthesia.

Heme oxygenase 1 (HO-1), induced by a variety of stressors, provides endogenous carbon monoxide (CO) and bilirubin, both of which play consequential roles in organs. The current study aimed to examine whether induction of HO-1 and its by-products modulated endothelial interaction with circulating leukocytes and platelets evoked by sevoflurane anesthesia in vivo. Rats, pretreated with or without hemin, were anesthetized with sevoflurane in 100% O2, and lungs were mechanically ventilated. Platelets labeled with carboxyfluorescein diacetate succinimidyl ester and leukocyte behavior in mesenteric venules were visualized during sevoflurane anesthesia at 1,000 frames/s using intravital ultrahigh-speed intensified fluorescence videomicroscopy. To examine the mechanisms for the effects of HO-1 on leukocyte and platelet behavior, these studies were repeated with superfusion of either CO, bilirubin, or Nomega-nitro-L-arginine methyl ester (L-NAME). As reported previously, the elevation of sevoflurane concentration evoked adhesive responses of leukocytes, concurrent with platelet margination and rolling. Pretreatment with hemin, a HO-1 inducer, prevented such sevoflurane-elicited changes in the microvessels. These changes were restored by zinc protoporphyrin IX, a HO inhibitor, and repressed by CO but not by bilirubin. During sevoflurane anesthesia, however, nitric oxide suppression by L-NAME deteriorated microvascular flows irrespective of the presence or absence of the HO-1 induction. These results indicate that endogenous CO via HO-1 induction attenuates sevoflurane-induced microvascular endothelial interactions with leukocytes and platelets, although local nitric oxide levels appear to dominate microvascular flow in situ.