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The European Respiratory Journal Jan 2017This document provides an update to the European Respiratory Society (ERS)/American Thoracic Society (ATS) technical standards for single-breath carbon monoxide uptake...
This document provides an update to the European Respiratory Society (ERS)/American Thoracic Society (ATS) technical standards for single-breath carbon monoxide uptake in the lung that was last updated in 2005. Although both D (diffusing capacity) and T (transfer factor) are valid terms to describe the uptake of carbon monoxide in the lung, the term D is used in this document. A joint taskforce appointed by the ERS and ATS reviewed the recent literature on the measurement of D and surveyed the current technical capabilities of instrumentation being manufactured around the world. The recommendations in this document represent the consensus of the taskforce members in regard to the evidence available for various aspects of D measurement. Furthermore, it reflects the expert opinion of the taskforce members on areas in which peer-reviewed evidence was either not available or was incomplete. The major changes in these technical standards relate to D measurement with systems using rapidly responding gas analysers for carbon monoxide and the tracer gas, which are now the most common type of D instrumentation being manufactured. Technical improvements and the increased capability afforded by these new systems permit enhanced measurement of D and the opportunity to include other optional measures of lung function.
Topics: Advisory Committees; Carbon Monoxide; Europe; Humans; Linear Models; Lung; Practice Guidelines as Topic; Pulmonary Diffusing Capacity; Reference Values; Societies, Medical; United States
PubMed: 28049168
DOI: 10.1183/13993003.00016-2016 -
Chembiochem : a European Journal of... Apr 2022Nitrogenases are the only known family of enzymes that catalyze the reduction of molecular nitrogen (N ) to ammonia (NH ). The N reduction drives biological nitrogen... (Review)
Review
Nitrogenases are the only known family of enzymes that catalyze the reduction of molecular nitrogen (N ) to ammonia (NH ). The N reduction drives biological nitrogen fixation and the global nitrogen cycle. Besides the conversion of N , nitrogenases catalyze a whole range of other reductions, including the reduction of the small gaseous substrates carbon monoxide (CO) and carbon dioxide (CO ) to hydrocarbons. However, it remains an open question whether these 'side reactivities' play a role under environmental conditions. Nonetheless, these reactivities and particularly the formation of hydrocarbons have spurred the interest in nitrogenases for biotechnological applications. There are three different isozymes of nitrogenase: the molybdenum and the alternative vanadium and iron-only nitrogenase. The isozymes differ in their metal content, structure, and substrate-dependent activity, despite their homology. This minireview focuses on the conversion of CO and CO to methane and higher hydrocarbons and aims to specify the differences in activity between the three nitrogenase isozymes.
Topics: Carbon Dioxide; Carbon Monoxide; Hydrocarbons; Isoenzymes; Nitrogen; Nitrogenase; Oxidation-Reduction
PubMed: 34643977
DOI: 10.1002/cbic.202100453 -
Medicina (Kaunas, Lithuania) Apr 2021Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle... (Review)
Review
Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle Ages, and usually ended fatally, was first successfully treated in the last century. Since then, diagnostics and treatments have undergone exciting developments, in particular specific treatments such as hyperbaric oxygen therapy. In this review, different historic aspects of the etiology, diagnosis and treatment of carbon monoxide intoxication are described and discussed.
Topics: Carbon Monoxide; Carbon Monoxide Poisoning; Fires; Humans; Hyperbaric Oxygenation; Middle Aged
PubMed: 33919037
DOI: 10.3390/medicina57050400 -
Journal of Advanced Research May 2022Endogenous gasotransmitters are small gaseous mediators that can be generated endogenously by mammalian organisms. The dysregulation of the gasotransmitter system is... (Review)
Review
BACKGROUND
Endogenous gasotransmitters are small gaseous mediators that can be generated endogenously by mammalian organisms. The dysregulation of the gasotransmitter system is associated with numerous disorders ranging from inflammatory diseases to cancers. However, the relevance of these endogenous gasotransmitters, prodrug donors and inhibitors in inflammatory dermatological disorders has not yet been thoroughly reviewed and discussed.
AIM OF REVIEW
This review discusses the recent progress and will provide perspectives on endogenous gasotransmitters in the context of inflammatory dermatological disorders.
KEY SCIENTIFIC CONCEPTS OF REVIEW
Endogenous gasotransmitters nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (HS) are signaling molecules that regulate several physiological and pathological processes. In addition, sulfur dioxide (SO₂), methane (CH), hydrogen gas (H), ammonia (NH), and carbon dioxide (CO) can also be generated endogenously and may take part in physiological and pathological processes. These signaling molecules regulate inflammation, vasodilation, and oxidative stress, offering therapeutic potential and attracting interest in the field of inflammatory dermatological disorders including psoriasis, atopic dermatitis, acne, rosacea, and chronic skin ulcers. The development of effective gas donors and inhibitors is a promising alternative to treat inflammatory dermatological disorders with controllable and precise delivery in the future.
Topics: Animals; Carbon Monoxide; Gasotransmitters; Hydrogen Sulfide; Mammals; Nitric Oxide; Signal Transduction; Sulfur Dioxide
PubMed: 35572410
DOI: 10.1016/j.jare.2021.08.012 -
Biochemical Pharmacology Aug 2022Carbon monoxide is quickly moving past its historic label as a molecule once feared, to a therapeutic drug that modulates inflammation. The development of carbon... (Review)
Review
Carbon monoxide is quickly moving past its historic label as a molecule once feared, to a therapeutic drug that modulates inflammation. The development of carbon monoxide releasing molecules and utilization of heme oxygenase-1 inducers have shown carbon monoxide to be a promising therapy in reducing renal ischemia and reperfusion injury and other inflammatory diseases. In this review, we will discuss the developments and application of carbon monoxide releasing molecules in renal ischemia and reperfusion injury, and transplantation. We will review the anti-inflammatory mechanisms of carbon monoxide in respect to mitigating apoptosis, suppressing dendritic cell maturation and signalling, inhibiting toll-like receptor activation, promoting anti-inflammatory responses, and the effects on renal vasculature.
Topics: Anti-Inflammatory Agents; Carbon Monoxide; Humans; Ischemia; Kidney Diseases; Reperfusion Injury
PubMed: 35777450
DOI: 10.1016/j.bcp.2022.115156 -
British Journal of Pharmacology Mar 2015Haem oxygenase (HO) and its product carbon monoxide (CO) are associated with cytoprotection and maintenance of homeostasis in several different organs and tissues. This... (Review)
Review
Haem oxygenase (HO) and its product carbon monoxide (CO) are associated with cytoprotection and maintenance of homeostasis in several different organs and tissues. This review focuses upon the role of exogenous and endogenous CO (via HO activity and expression) in various CNS pathologies, based upon data from experimental models, as well as from some clinical data on human patients. The pathophysiological conditions reviewed are cerebral ischaemia, chronic neurodegenerative diseases (Alzheimer's and Parkinson's diseases), multiple sclerosis and pain. Among these pathophysiological conditions, a variety of cellular mechanisms and processes are considered, namely cytoprotection, cell death, inflammation, cell metabolism, cellular redox responses and vasomodulation, as well as the different targeted neural cells. Finally, novel potential methods and strategies for delivering exogenous CO as a drug are discussed, particularly approaches based upon CO-releasing molecules, their limitations and challenges. The diagnostic and prognostic value of HO expression in clinical use for brain pathologies is also addressed.
Topics: Animals; Carbon Monoxide; Cell Death; Central Nervous System Diseases; Heme Oxygenase (Decyclizing); Homeostasis; Humans; Prognosis
PubMed: 24758548
DOI: 10.1111/bph.12729 -
American Journal of Physiology. Cell... Feb 2018Carbon monoxide (CO) is an endogenously produced gas that has gained recognition as a biological signal transduction effector with properties similar, but not identical,... (Review)
Review
Carbon monoxide (CO) is an endogenously produced gas that has gained recognition as a biological signal transduction effector with properties similar, but not identical, to that of nitric oxide (NO). CO, which binds primarily to heme iron, may activate the hemoprotein guanylate cyclase, although with lower potency than NO. Furthermore, CO can modulate the activities of several cellular signaling molecules such as p38 MAPK, ERK1/2, JNK, Akt, NF-κB, and others. Emerging studies suggest that mitochondria, the energy-generating organelle of cells, represent a key target of CO action in eukaryotes. Dose-dependent modulation of mitochondrial function by CO can result in alteration of mitochondrial membrane potential, mitochondrial reactive oxygen species production, release of proapoptotic and proinflammatory mediators, as well as the inhibition of respiration at high concentration. CO, through modulation of signaling pathways, can impact key biological processes including autophagy, mitochondrial biogenesis, programmed cell death (apoptosis), cellular proliferation, inflammation, and innate immune responses. Inhaled CO is widely known as an inhalation hazard due to its rapid complexation with hemoglobin, resulting in impaired oxygen delivery to tissues and hypoxemia. Despite systemic and cellular toxicity at high concentrations, CO has demonstrated cyto- and tissue-protective effects at low concentration in animal models of organ injury and disease. These include models of acute lung injury (e.g., hyperoxia, hypoxia, ischemia-reperfusion, mechanical ventilation, bleomycin) and sepsis. The success of CO as a candidate therapeutic in preclinical models suggests potential clinical application in inflammatory and proliferative disorders, which is currently under evaluation in clinical trials.
Topics: Animals; Carbon Monoxide; Dose-Response Relationship, Drug; Humans; Lung; Lung Diseases; Mitochondria; Signal Transduction
PubMed: 29118026
DOI: 10.1152/ajpcell.00022.2017 -
Medical Gas Research 2020Nitric oxide, studied to evaluate its role in cardiovascular physiology, has cardioprotective and therapeutic effects in cellular signaling, mitochondrial function, and... (Review)
Review
Nitric oxide, studied to evaluate its role in cardiovascular physiology, has cardioprotective and therapeutic effects in cellular signaling, mitochondrial function, and in regulating inflammatory processes. Heme oxygenase (major role in catabolism of heme into biliverdin, carbon monoxide (CO), and iron) has similar effects as well. CO has been suggested as the molecule that is responsible for many of the above mentioned cytoprotective and therapeutic pathways as CO is a signaling molecule in the control of physiological functions. This is counterintuitive as toxic effects are related to its binding to hemoglobin. However, CO is normally produced in the body. Experimental evidence indicates that this toxic gas, CO, exerts cytoprotective properties related to cellular stress including the heart and is being assessed for its cytoprotective and cytotherapeutic properties. While survival of adult cardiomyocytes depends on oxidative phosphorylation (survival and resulting cardiac function is impaired by mitochondrial damage), mitochondrial biogenesis is modified by the heme oxygenase-1/CO system and can result in promotion of mitochondrial biogenesis by associating mitochondrial redox status to the redox-active transcription factors. It has been suggested that the heme oxygenase-1/CO system is important in differentiation of embryonic stem cells and maturation of cardiomyocytes which is thought to mitigate progression of degenerative cardiovascular diseases. Effects on other cardiac cells are being studied. Acute exposure to air pollution (and, therefore, CO) is associated with cardiovascular mortality, myocardial infarction, and heart failure, but changes in the endogenous heme oxygenase-1 system (and, thereby, CO) positively affect cardiovascular health. We will review the effect of CO on heart health and function in this article.
Topics: Animals; Carbon Monoxide; Heart; Humans
PubMed: 32189668
DOI: 10.4103/2045-9912.279982 -
Chemical Communications (Cambridge,... Apr 2014Carbon monoxide (CO) is increasingly recognized as a cell-signalling molecule akin to nitric oxide (NO). CO has attracted particular attention as a potential therapeutic... (Review)
Review
Carbon monoxide (CO) is increasingly recognized as a cell-signalling molecule akin to nitric oxide (NO). CO has attracted particular attention as a potential therapeutic agent because of its reported anti-hypertensive, anti-inflammatory and cell-protective effects. We discuss recent progress in identifying new effector systems and elucidating the mechanisms of action of CO on, e.g., ion channels, as well as the design of novel methods to monitor CO in cellular environments. We also report on recent developments in the area of CO-releasing molecules (CORMs) and materials for controlled CO application. Novel triggers for CO release, metal carbonyls and degradation mechanisms of CORMs are highlighted. In addition, potential formulations of CORMs for targeted CO release are discussed.
Topics: Animals; Carbon Monoxide; Coordination Complexes; Delayed-Action Preparations; Humans
PubMed: 24556640
DOI: 10.1039/c3cc49196j -
Biochemical Pharmacology Jul 2022Gastrointestinal (GI) tract cancers pose a significant pharmacological challenge for researchers in terms of the discovery of molecular agents and the development of... (Review)
Review
Gastrointestinal (GI) tract cancers pose a significant pharmacological challenge for researchers in terms of the discovery of molecular agents and the development of targeted therapies. Although many ongoing clinical trials have brought new perspectives, there is still a lack of successful long-term treatment. Several novel pharmacological and molecular agents are being studied in the prevention and treatment of GI cancers. On the other hand, pharmacological tools designed to release an endogenous gaseous mediator, carbon monoxide (CO), were shown to prevent the gastric mucosa against various types of injuries and exert therapeutic properties in the treatment of GI pathologies. In this review, we summarized the current evidence on the role of CO and heme oxygenase 1 (HO-1) as a CO producing enzyme in the pathophysiology of GI tumors. We focused on a beneficial role of HO-1 and CO in biological systems and common pathological conditions. We further discussed the complex and ambiguous function of the HO-1/CO pathway in cancer cells with a special emphasis on molecular and cellular pro-cancerous and anti-cancer mechanisms. We also focused on the role that HO-1/CO plays in GI cancers, especially within upper parts such as esophagus or stomach.
Topics: Carbon Monoxide; Gastric Mucosa; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Heme Oxygenase (Decyclizing); Heme Oxygenase-1; Humans
PubMed: 35490732
DOI: 10.1016/j.bcp.2022.115058