Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARBON MONOXIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1982

[Occurrence of carbon monoxide, carbon dioxide and nitrogen oxides during the use of gas stoves].

The concentrations of carbon monoxide, carbon dioxide, nitrogen monoxide and nitrogen dioxide arising from gas burning have been measured under experimental and field conditions. In the test room propane, butane and town-gas have been burned, whereas in the apartments investigated only town-gas has been used. The most important influence on the concentration of the four substances arises from the changes in the burning conditions of the flame. Laboratory experiments have been carried out in the test room with open flames and with an aluminum block or a kettle on the flame. The following results have been obtained: (a) for CO the lowest concentration is obtained with open flames irrespective of the type of gas burned. Higher concentrations have been found with aluminum blocks, whereas the highest concentrations were associated with the use of kettles and pots, (b) the experimental conditions have only a small influence on the CO2 concentration, (c) NO concentrations are influenced by the gas type and by the experimental conditions. They are low with kettles but high with open flames, (d) NO2 concentrations are less influenced by the experimental conditions than are NO concentrations. The results of more than 1000 paired determinations of NO2 in kitchen and other rooms are presented. The concentrations which have been measured using diffusion tubes according to Palmes which were exposed for 48 h, were highest in kitchens of dwellings fully equipped with gas devices (heating, cooking, warming water). The mean value of the concentrations was about 50 micrograms/m3, whereas the mean for dwellings without any gas device has been found to be lower than 20 micrograms/m3.

Air Pollutants↗
PubMed1989

Carbon monoxide, carbon disulfide, lead and cadmium--four examples of occupational toxic agents linked to cardiovascular disease.

A variety of industrial agents to which large segments of the population are exposed have been linked to the development of cardiovascular disease. These toxic agents, which include carbon monoxide, carbon disulphide, lead, and cadmium, are produced by a wide variety of industrial processes and so are ubiquitous in the modern industrial environment. Although the mechanisms by which such toxins may contribute to cardiovascular disease are not well defined, there are at least four possible theories that have received clinical and experimental support. The postulated mechanisms by which such toxins may play a role in vascular disease are: (1) an increase in blood pressure; (2) an increase in the levels of blood cholesterol and/or an induction of lipid accumulation in vessel walls; (3) an induction of a lipid peroxidation process thereby increasing the tendency of blood clotting; and (4) a promotion of a mutation in the arterial cell wall.

Animals↗
PubMed1985

Passive colorimetric dosimeter tubes for ammonia, carbon monoxide, carbon dioxide, hydrogen sulfide, nitrogen dioxide and sulfur dioxide.

Colorimetric, stain length, personal dosimeters operating by gas diffusion have been developed to determine worker exposure for up to an eight-hour period for several inorganic airborne contaminants in the range of their Threshold Limit Values. Length of stain, colorimetric dosimeters have been made for the detection of ammonia (NH3), carbon monoxide (CO), carbon dioxide (CO2), hydrogen sulfide (H2S), nitrogen dioxide (NO2), and sulfur dioxide (SO2) in air. For each gas detection system, the sampler depends on the transfer of the gas by diffusion into a glass tube containing a colorimetric length of stain indicator. The stain length developed in a given period of time is compared to a calibration chart to determine, on the spot, the average gas concentration to which the dosimeter has been exposed. These dosimeters are known by the trade name Vapor Gard.

Air Pollutants, Occupational↗
PubMed1984

Mechanism of the metabolism of 1,3-benzodioxoles to carbon monoxide.

Carbon monoxide is a minor product formed during the cytochrome P-450-catalyzed oxidation of 1,3-benzodioxoles. Studies with [2-13C]methylene 1,3-benzodioxoles established that the methylenic carbon of the 1,3-benzodioxole ring is the source of the carbon atom in the carbon monoxide, and an isotope effect of 1.7 to 2.0 was observed with [2-2H2]methylene derivatives. Incubations conducted in the presence of [18O]dioxygen and [18O]water showed that the oxygen atom in carbon monoxide arises from both oxygen and water. A mechanism consistent with these data has been proposed for carbon monoxide formation. It involves initial monooxygenation of the 1,3-benzodioxole to a 2-hydroxy derivative that subsequently forms a 2-hydroxyphenyl formate intermediate, which yields either carbon monoxide or formate. The proposed mechanism is discussed in terms of its possible relationship to the inhibitory activity of 1,3-benzodioxoles toward microsomal oxidation.

Animals↗
PubMedDate not supplied

Some usual and unusual poisonings due to carbon monoxide.

Carbon monoxide poisoning is a frequent occurrence in both developed and under developed countries of the world. Carbon monoxide can be produced in fires, automobile engine exhausts and the incomplete combustion of organic matter. It is a "silent killer" that initially produces a mild progressive frontal headache, drowsiness and sleep that is usually ignored as common place. Continued low-level CO exposure for a long period of time in a confined space is cumulative and these accidental deaths are frequent but should be avoidable. Several usual and unusual poisonings are reported to illustrate its various forms of exposure. It all began many years ago when a bolt of lightening hit a fallen tree and produced a fire. Early cave man later learned to enjoy some of the benefits of this new discovery. They could now see at night, they could keep warm, keep the predators at bay, cook their food and make it taste better and be more gentle to their teeth. Also meat could be preserved and eaten at a later date especially if it were dried and smoked. They learned by trial and error that it was dangerous to bring their fire deep into their cave without a chimney. Carbon monoxide (CO) also can be easily produced by many other sources besides fire. Very common today is the incomplete combustion of gasoline in the engine of an automobile which can produce about 6% carbon monoxide.

Accidents↗
PubMedDate not supplied

Anthropogenic emissions of carbon monoxide.

Carbon monoxide (CO) is a colorless, nonirritating, odorless and tasteless gas. Carbon monoxide combines with hemoglobin far more readily than does oxygen, leading to tissue hypoxia. Thousands of people die annually from CO poisoning, and those recovering from acute exposure commonly suffer brain damage. Chronic poisoning is of particular concern to sufferers of coronary heart disease, pregnant women, and people with certain hematological disorders. Indoor emission sources, notably fuel-burning heating appliances, cause most unintentional deaths and cases of illness and should be the main focus of concern. Motor vehicle emissions pose a chronic health risk for occupationally exposed groups. Smoking is a major source of personal exposure. Recent exposure to CO is commonly evaluated by measuring blood carboxyhemoglobin levels, which are related to the concentration of atmospheric CO. Monitoring methods are reviewed here, and monitoring is considered in relation to air quality standards and guidelines. Finally, control measures for motor vehicles and indoor heating appliances are suggested.

Adult↗
PubMed2003

The clinical toxicology of carbon monoxide.

Carbon monoxide (CO) is a dangerous exogenous poison and an essential endogenous neurotransmitter. This gas when inhaled has an anaesthetic effect, which is poorly understood, but which may be fatal if compensatory mechanisms are exhausted, if cardiac oxygen (O(2)) needs exceed myocardial oxygenation and/or if apnoea or asphyxia onsets. Although there is considerable evidence that hypoxia occurs late in CO poisoning, both the treatment of acutely poisoned people and environmental exposure limits are largely based on a hypoxic theory of toxicity. The significance of recent demonstrations of increased endogenous CO and NO production in neurons of animals exposed to exogenous CO, and of a related sequestration of leucocytes along the endothelium and subsequent diapedesis is also not fully understood, but may in part explain both acute and delayed deleterious effects of a CO exposure. Delayed brain injuries due to a CO exposure may be preventable by hyperbaric O(2). However, the ideal dose of O(2) in this context, if any, is unknown and other potential treatments need to be tested.

Animals↗
PubMed2003

Infrared studies of carbon monoxide binding to carbon monoxide dehydrogenase/acetyl-CoA synthase from Moorella thermoacetica.

Carbon monoxide dehydrogenase/acetyl-CoA synthase (CODH/ACS) is a bifunctional enzyme that catalyzes the reversible reduction of carbon dioxide into carbon monoxide and the coupled synthesis of acetyl-CoA from the carbon monoxide produced. Exposure of CODH/ACS from Moorella thermoacetica to carbon monoxide gives rise to several infrared bands in the 2100-1900 cm(-1) spectral region that are attributed to the formation of metal-coordinated carbon monoxide species. Infrared bands attributable to M-CO are not detected in the as-isolated enzyme, suggesting that the enzyme does not contain intrinsic metal-coordinated CO ligands. A band detected at 1996 cm(-1) in the CO-flushed enzyme is assigned as arising from CO binding to a metal center in cluster A of the ACS subunit. The frequency of this band is most consistent with it arising from a terminally coordinated Ni(I) carbonyl. Multiple infrared bands at 2078, 2044, 1970, 1959, and 1901 cm(-1) are attributed to CO binding at cluster C of the CODH subunit. All infrared bands attributed to metal carbonyls decay in a time-dependent fashion as CO(2) appears in the solution. These observations are consistent with the enzyme-catalyzed oxidation of carbon monoxide until it is completely depleted from solution during the course of the experiments.

Acetate-CoA Ligase↗
PubMed1993

Activation of whole cell currents in isolated human jejunal circular smooth muscle cells by carbon monoxide.

Carbon monoxide (CO) is a low molecular weight oxide produced endogenously from fatty acids and heme protein. A physiological role for CO has been suggested for vascular smooth muscle, hemostasis, and olfactory neurons, but direct evidence is lacking. Heme oxygenase, which catalyzes the formation of CO from heme proteins, is present in small intestinal smooth muscle. The effect of 1% CO on whole cell currents in normal human jejunal circular muscle cells was studied with the use of a perforated patch-clamp technique. A 1% CO-containing Krebs solution caused an initial and transient increase in whole cell current in 20 of 22 cells tested (175 +/- 40%, mean +/- SE) and a transient hyperpolarization (15.6 +/- 3.6 mV, mean +/- SE) of the membrane potential. During prolonged recordings, 1% CO evoked ongoing cyclic increases and decreases in the whole cell current. Each current increase was accompanied by a sharp membrane hyperpolarization. These data suggest that CO may modulate whole cell potassium current and membrane potential.

Carbon Monoxide↗
PubMed2002

Biological chemistry of carbon monoxide.

Carbon monoxide (CO) has many effects in biology due to its complex biochemical activities. These actions of CO depend primarily on its ability to bind heme proteins (Hp) and to inhibit or alter their biochemical functions. Whether CO is derived from exogenous or endogenous sources, its cellular activity is related to its concentration and the concentration of molecular O(2), as well as to the availability of reduced transition metals such as Fe(II). In this respect, the CO/O(2) ratio and O(2)-dependent changes in local oxidation-reduction state assume critical importance in determining the physiological effects of CO by affecting the functions of specific Hp. By interacting with Hp, CO influences electron-transport reactions in a variety of ways, which can produce either prooxidant or antioxidant effects. Similarly, Hp relationships also govern how changes in CO concentration influence the physiological and pathological effects of nitric oxide and the relationships of the two biologically active gases to metal-catalyzed oxidations. This article provides a brief update on the biochemistry of CO as it relates to Hp binding, chemical oxidative processes, and cellular function.

Animals↗
PubMed2001

The vasorelaxation of cerebral arteries by carbon monoxide.

Carbon monoxide (CO) is known to increase cerebral blood flow, but the effect of CO on the vascular tone of large cerebral arteries is uncertain. We tested whether CO affects cerebral artery tone by measuring tension generated by ex vivo segments of dog basilar artery upon exposure to CO. In cerebral artery segments contracted with either KCl or prostaglandin F(2alpha), CO caused a concentration-related relaxation beginning with a concentration of 57 microM. Relaxation did not occur if CO was administered in the presence of bubbling carboxygen (95% O(2):5% CO(2)), which reduces greater than 99% of CO from the solution. Furthermore, the CO-induced relaxation of cerebral artery segments was reduced in the presence of the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 microM)or the potassium channel blocker tetraethylammonium (TEA, 1 mM). Neither ODQ nor TEA completely eliminated the relaxation caused by CO and there was no additive effect if ODQ and TEA were administered together. These results suggest that cerebral arteries are directly relaxed by CO and that this relaxation depends upon the activation of guanylyl cyclase and the opening of potassium channels.

Animals↗
PubMed2004

Protection of transplant-induced renal ischemia-reperfusion injury with carbon monoxide.

Carbon monoxide (CO), a product of heme metabolism by heme oxygenases, is known to impart protection against oxidative stress. We hypothesized that CO would protect ischemia-reperfusion (I/R) injury of transplanted organs, and the efficacy of CO was studied in the rat kidney transplantation model. A Lewis rat kidney graft, preserved in University of Wisconsin solution at 4 degrees C for 24 h, was orthotopically transplanted into syngeneic rats. Recipients were maintained in room air or exposed to CO (250 ppm) in air for 1 h before and 24 h after transplantation. Animals were killed 1, 3, 6, and 24 h after transplantation to assess efficacy of inhaled CO. Rapid upregulation of mRNA for IL-6, IL-1beta, TNF-alpha, ICAM-1, heme oxygenase-1, and inducible nitric oxide synthase was observed within 3 h after transplantation in the control grafts of air-exposed recipients, associating with histopathological evidences of acute tubular necrosis, interstitial hemorrhage, and edema. In contrast, the increase of inflammatory mediators was markedly inhibited in kidney grafts of CO-treated recipients, which correlated with improved renal cortical blood flow. Further detailed morphological analyses revealed that CO preserved the glomerular vascular architecture and podocyte viability with less apoptosis of tubular epithelial cells and less ED1(+) macrophage infiltration. CO inhalation resulted in improved serum creatinine levels and clearance, and animal survival was significantly improved with CO to 60.5 from 25 days in untreated controls. The study demonstrates that exposure of kidney graft recipients to CO at a low concentration can impart significant protective effects against renal I/R injury and improve function of renal grafts.

Actins↗