Carbon Monoxide Poisoning

Chenoweth, James A.; Albertson, Timothy E; Greer, Matthew R.

doi:10.1016/j.ccc.2021.03.010

Cited by 47 publications

(34 citation statements)

References 62 publications

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“…Carbon monoxide (CO) exposure is an established approach to reduce tissue oxygenation, which has been linked to cytoprotective effects as well as oxidative stress induction. 138 , 139 Although various positive effects were observed ( Supplementary Table 2 ), chronic CO exposure induced hyperintense lesions in the caudoputamen region of the brain in Ndufs4 −/− -WB mice, indicative of adverse effects. 137 Similarly, hypoxic conditions prevented/mitigated part of the disease phenotype in Ndufs4 −/− -WB mice (prolonged lifespan, no loss of body weight, improved motor function, prevention of hypothermia).…”

Section: Intervention Studies In Ndufs4 Mouse Modelsmentioning

confidence: 99%

Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention

Wal

Adjobo‐Hermans

Keijer

et al. 2021

Brain

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Mitochondria are small cellular constituents that generate cellular energy (ATP) by oxidative phosphorylation (OXPHOS). Dysfunction of these organelles is linked to a heterogeneous group of multisystemic disorders, including diabetes, cancer, ageing-related pathologies and rare mitochondrial diseases (MDs). With respect to the latter, mutations in subunit-encoding genes and assembly factors of the first OXPHOS complex (CI) induce isolated CI deficiency and Leigh syndrome (LS). This syndrome is an early-onset, often fatal, encephalopathy with a variable clinical presentation and poor prognosis due to the lack of effective intervention strategies. Mutations in the nuclear DNA (nDNA)-encoded NDUFS4 gene, encoding the NADH: Ubiquinone oxidoreductase subunit S4 (NDUFS4) of CI induce “mitochondrial complex I deficiency, nuclear type 1” (MC1DN1) and LS in pediatric patients. A variety of (tissue-specific) Ndufs4 knockout mouse models were developed to study the LS pathomechanism and intervention testing. Here, we review and discuss the role of CI and NDUFS4 mutations in human MD, and review how the analysis of Ndufs4 knockout mouse models has generated new insights into the MC1ND1/LS pathomechanism and its therapeutic targeting.

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Section: Intervention Studies In Ndufs4 Mouse Modelsmentioning

confidence: 99%

Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention

Wal

Adjobo‐Hermans

Keijer

et al. 2021

Brain

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“…In addition, CO binds to platelet heme protein, causing the release of NO. Increased NO produces peroxynitrite (ONOO), which impairs mitochondrial function and worsens tissue hypoxia [5]. The central nervous system are most vulnerable to the effects of ischaemia and hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Isolated unilateral brachial plexus injury following carbon monoxide intoxication: a case report

Liu

Sun

et al. 2023

Preprint

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Background CO is an odorless, colorless gas that often still undetectable until exposure results in coma or death. Carbon monoxide (CO) intoxication is a common fatal poisoning worldwide. The toxic effects of CO lead to tissue hypoxia and produce systemic and neurological complications. Besides, some severe neurological manifestations and delayed sequelae may occur after CO intoxication. However, peripheral neuropathy following CO poisoning is relatively rare that usually occurs in young people. Beforehand, only one case reported unilateralplexopathy following CO poisoning, which combined with rhabdomyolysis and cognitive dysfunction. Case presentation A 31-year-old young man slept in his private car with closed doors and windows. His wife discovered him in about 7 hours when he was in an unconscious state. He was diagnosed with acute carbon monoxide poisoning. After about 12 hours in a coma, he returned to an alert state without conscious disorder. However, he woke up with left upper arm weakness associated with limitation of movement of the left upper limb. The electrophysiological conclusion was left incomplete total brachial plexopathy. Conclusion Ischemia of spinal cordcaused by CO intoxication may be a key mechanism in this case. Hyperbaric oxygen therapy as soon as possible is necessary to prevent peripheral neuropathy after acute CO intoxication. Besides, persisting in rehabilitation training might be important to treat peripheral neuropathy after acute CO intoxication.

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“…Carbon monoxide (CO) poisoning is one of the most common causes of fatal poisoning worldwide. Long-term exposure to potentially lethal doses of CO exceeding 100 ppm can cause poisoning; CO is produced by internal combustion engines, fossil fuel furnaces and fire and is toxic ( 1 ). Although the CO emissions of modern cars are controlled by regulatory standards, they remain highly toxic in poorly ventilated environments.…”

Section: Introductionmentioning

confidence: 99%

Burden of carbon monoxide poisoning in China, 1990–2019: A systematic analysis of data from the global burden of disease study 2019

Cui

Yan

Feng³

et al. 2022

Front. Public Health

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BackgroundCarbon monoxide (CO) poisoning is one of the most common toxic occupational diseases, but related data in China are scarce. A better understanding of the burden of CO poisoning is essential for improving its management.MethodsA systematic analysis of data from the Global Burden of Disease (GBD) Study 2019 was conducted. Following the general analytical strategy used in the GBD Study 2019, the sex- and age-specific incidence and mortality rates of CO poisoning and disability-adjusted life years (DALYs) due to CO poisoning in China were analyzed. Estimated average annual percentage changes (AAPCs) in age-standardized rates were calculated by joinpoint regression analysis. The effects of age, period and cohort on the incidence of CO poisoning and DALYs due to CO poisoning were estimated by an age-period-cohort model.ResultsThe age-standardized incidence and mortality rates as well as DALYs of CO poisoning per 100,000 population were estimated to be 21.82 [95% uncertainty interval (UI): 15.05–29.98], 0.93 (95% UI: 0.63–1.11), and 40.92 (95% UI: 28.43–47.85), respectively, in 2019. From 1990 to 2019, the AAPCs in the age-standardized incidence significantly increased in both males and females, while the age-standardized mortality rates and DALYs significantly decreased in both males and females. The incidence of CO poisoning peaked in individuals aged 15–19 years. Males had a higher burden of CO poisoning than females. The age effect showed that the relative risks (RRs) of incident CO poisoning decreased with age among males and females and that individuals aged 15–24 years had the highest RRs. The RRs of incident CO poisoning increased with time. The cohort effect showed that the incidence increased in successive birth cohorts.ConclusionsThe incidence of CO poisoning in China increased from 1990 to 2019. More attention should be given to improving the burden of CO poisoning in Chinese adolescents. The results of this study can be used by health authorities to inform preventative measures to reduce the burden of CO poisoning.

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Carbon Monoxide Poisoning

Cited by 47 publications

References 62 publications

Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention

Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention

Isolated unilateral brachial plexus injury following carbon monoxide intoxication: a case report

Burden of carbon monoxide poisoning in China, 1990–2019: A systematic analysis of data from the global burden of disease study 2019

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