Relative Affinity of Hemoglobin S and Hemoglobin A for Carbon Monoxide and Oxygen

Rodkey, F. Lee; O’Neal, John D.; Collison, Harold A.; Uddin, David E.

doi:10.1093/clinchem/20.1.83

Cited by 82 publications

(30 citation statements)

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“…However, we found that COHb concentration was not a predictive factor for DNS, similar to several other reports . The affinity of hemoglobin for CO is approximately 220 times greater than that for oxygen . Therefore, CO rapidly binds to hemoglobin after exposure and is transferred to the intracellular space where it binds myoglobin and mitochondrial cytochrome oxidase .…”

Section: Discussionsupporting

confidence: 87%

Risk factors for the delayed onset of neuropsychologic sequelae following carbon monoxide poisoning

Kitamoto

Tsuda

Kato

et al. 2016

Acute Medicine & Surgery

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AimCarbon monoxide (CO) poisoning often manifests delayed neuropsychological sequelae. The risks and preventive factors for the development of delayed neuropsychological sequelae are controversial at present. The purpose of this retrospective study was to assess the risk factors for this condition.MethodWe studied 81 patients with CO poisoning admitted to the Critical Care and Emergency Medicine Center at the Kansai Medical University from 2006 to 2012. All patients (64 males and 17 females; average age, 45.9 years) were divided into non‐ delayed neuropsychological sequelae and delayed neuropsychological sequelae groups and retrospectively studied. Patient data were analyzed by univariate and multivariate analyses.ResultsThe results of our study indicated that prolonged CO exposure, elevated serum creatinine phosphokinase levels, head image abnormality in the basal ganglion or white matter region, low Glasgow Coma Scale score, bedsore occurrence, and CO poisoning attributable to burning charcoal were each predictive risk factors for the development of delayed neuropsychological sequelae. Bedsore occurrence and serum creatinine phosphokinase elevation were significant risk factors by multivariate analysis, whereas no significant differences were found for age, gender, mean blood pressure, heart rate, arterial carboxyhemoglobin and lactate concentrations, or base excess.ConclusionWe identified several predictive risk factors of delayed neuropsychological sequelae. We believe that these factors will contribute to identifying optimum therapeutic methods and follow‐up terms for patients with acute CO poisoning at risk of developing delayed neuropsychological sequelae.

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Section: Discussionsupporting

confidence: 87%

Risk factors for the delayed onset of neuropsychologic sequelae following carbon monoxide poisoning

Kitamoto

Tsuda

Kato

et al. 2016

Acute Medicine & Surgery

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“…Such a disturbance of mitochondrial respiratory chain function could lead to a decay in mitochondria energy production and, eventually, to cellular injury or dysfunction, especially in “high metabolic rate” tissues exposed to CO such as the central nervous system, heart muscle or skeletal muscle. Indeed, muscular weakness and impaired heart function have been reported and demonstrated in CO poisoning (Tritapepe et al 1998; Raub et al 2000; Yanir et al 2002) and in heavy smokers (Örlander et al 1979; Gvozdjakova et al 1984). On the other hand, the disturbance in mitochondrial respiratory chain function may also lead to a major production of reactive oxygen species (Cadenas & Davis 2000).…”

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

Alonso

Cardellach

López

et al. 2003

Pharmacology & Toxicology

214

113

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Carbon monoxide (CO) toxicity is the result of a combination of tissue hypoxia and direct CO-mediated damage at a cellular level, since not all the signs and symptoms presented can be explained only by the formation of carboxyhaemoglobin. Mitochondria, specially the electron transport chain, seem to be the target for CO at a subcellular level. However, the direct effect of CO in individual complexes of the human mitochondrial respiratory chain has not been completely elucidated. We here studied the in vitro effect of CO on individual complexes of the mitochondrial respiratory chain of human mitochondria. We obtained muscle tissue from 10 healthy people who underwent orthopaedic surgery for hip replacement. Isolated mitochondria were incubated for 5 min. under CO concentrations of 50, 100 and 500 ppm. Afterwards, enzymatic activities of individual complexes of the mitochondrial respiratory chain were assessed in vitro and compared with those obtained in basal (synthetic air without CO) conditions. Cytochrome c oxidase (complex IV of the mitochondrial respiratory chain) activity showed a decrease from 836∫439 nmol/min

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“…Carbon monoxide (CO) is a potent vertebrate toxin that binds 200-300 times more tightly to haemoglobin than O 2 (Rodkey et al, 1974), blocking oxygenation of the tissues and inhibiting the mitochondrial electron transport chain by binding cytochromes, with potentially lethal effects. This toxicity extends even to the microbial world, with the ability of CO to bind to and inhibit metalloenzymes as well as interrupt electron transport chains.…”

Section: Introductionmentioning

confidence: 99%

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

Techtmann

Colman

Robb

2009

Environmental Microbiology

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SummaryCarbon 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 H2. 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 H2, CO2 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.

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Relative Affinity of Hemoglobin S and Hemoglobin A for Carbon Monoxide and Oxygen

Cited by 82 publications

References 0 publications

Risk factors for the delayed onset of neuropsychologic sequelae following carbon monoxide poisoning

Risk factors for the delayed onset of neuropsychologic sequelae following carbon monoxide poisoning

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

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

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