Nitrous oxide abuse in the emergency ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Permalink :
Title :
Nitrous oxide abuse in the emergency practice, and review of toxicity mechanisms and potential markers.
Author(s) :
Joncquel, Marie [Auteur]
Maladies Rares du Développement : Génétique, Régulation et Protéomique (RADEME) - ULR 7364
Grzych, Guillaume [Auteur]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U 1011 [RNMCD]
Récepteurs nucléaires, Maladies Cardiovasculaires et Diabète (EGID) - U1011
Tard, Celine [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Lannoy, Julien [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Deheul, Sylvie [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hanafi, Riyad [Auteur]
Services de neuroradiologie [Lille]
Douillard, Claire [Auteur]
Service Endocrinologie, diabétologie, maladies métaboliques et nutrition [LILLE - Endocrino]
Vamecq, Joseph [Auteur]
Maladies RAres du DEveloppement embryonnaire et du MEtabolisme : du Phénotype au Génotype et à la Fonction - ULR 7364 [RADEME]
Maladies Rares du Développement : Génétique, Régulation et Protéomique (RADEME) - ULR 7364
Grzych, Guillaume [Auteur]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U 1011 [RNMCD]
Récepteurs nucléaires, Maladies Cardiovasculaires et Diabète (EGID) - U1011
Tard, Celine [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Lannoy, Julien [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Deheul, Sylvie [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hanafi, Riyad [Auteur]
Services de neuroradiologie [Lille]
Douillard, Claire [Auteur]
Service Endocrinologie, diabétologie, maladies métaboliques et nutrition [LILLE - Endocrino]
Vamecq, Joseph [Auteur]
Maladies RAres du DEveloppement embryonnaire et du MEtabolisme : du Phénotype au Génotype et à la Fonction - ULR 7364 [RADEME]
Journal title :
Food and Chemical Toxicology
Abbreviated title :
Food Chem Toxicol
Pages :
112894
Publication date :
2022-03-02
ISSN :
1873-6351
English keyword(s) :
Biological markers
Homocysteine
Folate cycle
Methylation cycle
Methylmalonyl-CoA mutase
Methionine synthase
Vitamin B12
Cobalamins
Nitrous oxide abuse
Homocysteine
Folate cycle
Methylation cycle
Methylmalonyl-CoA mutase
Methionine synthase
Vitamin B12
Cobalamins
Nitrous oxide abuse
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Nitrous oxide (N2O) toxicity is a concern common to several medical fields. Here, retrospective study of four N2O abuses with neurological signs in the emergency practice provides a preliminary basis for a metabolic ...
Show more >Nitrous oxide (N2O) toxicity is a concern common to several medical fields. Here, retrospective study of four N2O abuses with neurological signs in the emergency practice provides a preliminary basis for a metabolic Discussion/Review. This latter highlights N2O abuse as pathology of DNA/RNA/protein methylations, for instance consistent with impairments of protein arginine methyltransferases involved in myelinogenesis and myelopathy in patients. Basically, pathogenesis starts with oxidation by N2O of coordinated cobalamine cobalt ions at enzyme sites with impairments of vitamin-B12-dependent pathways. Methionine synthase (methylcobalamine) and methymalonyl-CoA mutase (adenosylcobalamine) are inactivated and cofactor-depleted, respectively. The number of impacted pathways (folate cycle, methylation cycle, S-adenosylmethionine-dependent methyltransferases, transulfuration pathway, Krebs cycle fueling by methylmalonyl-CoA, glutathione synthesis) explains the variety of potential research/laboratory markers, and may provide new clues and future angles to explore N2O toxicity. Overall, homocysteine measurements obviously help diagnosis of N2O abuses. Additional markers may include vitamin-B12, methionine, methylmalonate, dimethylglycine, sarcosine, S-adenosylmethionine to S-adenosylhomocysteine ratio, various S-adenosylamino acids, S-adenosylmethionine-dependent cellular methylations, and additional analytes (propionylcarnitine, propionylglycine, cystathionine and derived metabolites, methylated amino acids [eg arginine], betaine).Show less >
Show more >Nitrous oxide (N2O) toxicity is a concern common to several medical fields. Here, retrospective study of four N2O abuses with neurological signs in the emergency practice provides a preliminary basis for a metabolic Discussion/Review. This latter highlights N2O abuse as pathology of DNA/RNA/protein methylations, for instance consistent with impairments of protein arginine methyltransferases involved in myelinogenesis and myelopathy in patients. Basically, pathogenesis starts with oxidation by N2O of coordinated cobalamine cobalt ions at enzyme sites with impairments of vitamin-B12-dependent pathways. Methionine synthase (methylcobalamine) and methymalonyl-CoA mutase (adenosylcobalamine) are inactivated and cofactor-depleted, respectively. The number of impacted pathways (folate cycle, methylation cycle, S-adenosylmethionine-dependent methyltransferases, transulfuration pathway, Krebs cycle fueling by methylmalonyl-CoA, glutathione synthesis) explains the variety of potential research/laboratory markers, and may provide new clues and future angles to explore N2O toxicity. Overall, homocysteine measurements obviously help diagnosis of N2O abuses. Additional markers may include vitamin-B12, methionine, methylmalonate, dimethylglycine, sarcosine, S-adenosylmethionine to S-adenosylhomocysteine ratio, various S-adenosylamino acids, S-adenosylmethionine-dependent cellular methylations, and additional analytes (propionylcarnitine, propionylglycine, cystathionine and derived metabolites, methylated amino acids [eg arginine], betaine).Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Université de Lille
CHU Lille
CHU Lille
Collections :
Submission date :
2023-06-05T07:08:49Z
2024-06-13T07:26:49Z
2024-06-13T07:26:49Z