MEGALOBLASTIC HÆMOPOIESIS IN PATIENTS RECEIVING NITROUS OXIDE

 in vitro, and probably also in vivo when premixed 50% nitrous oxide and 50% oxygen mixture ('Entonox') is given.

Toward adhesion-free endoscopy?

We believe that the adhesion prevention property of N2O is possibly related to its well-known side effects:

, inactivating the methionine synthase and causing a dose-dependent increase in plasma homocysteine (Hcys) concentrations.

Toxicity of nitrous oxide.

 resulting in selective inhibition of methionine synthase, a key enzyme in methionine and folate metabolism.

Homocysteine remethylation during nitrous oxide exposure of cells cultured in media containing various concentrations of folates.

, which serves as a cofactor of the enzyme methionine synthase catalyzing the remethylation of homocysteine to methionine.

Health hazards and nitrous oxide: a time for reappraisal.

, thereby inhibiting the action of methionine synthase, an enzyme that indirectly supports methylation reactions and nucleic acid synthesis.

Clinical aspects of the interaction between nitrous oxide and vitamin B12.

In 1968, Banks, Henderson and Pratt reported that

, converting the cobalt from the monovalent form (Cob(I)alamin) to the bivalent form (Cob(II)alamin), which can no longer function as a methyl carrier.

Clinical Pharmacokinetics of the Inhalational Anaesthetics

 and signs of megaloblastic bone marrow are present after 6 hours of anaesthesia.

The effects of nitrous oxide on cobalamins, folates, and on related events.

 from the active reduced cob[I]alamin form to the inactive cob[III]alamin form.

Cobalamins and nitrous oxide: a review.

 (N20), once regarded as chemically inert, oxidises some forms of 

[Thromboembolisms due to recreational use of nitrous oxide].

, leading to vitamin B12 deficiency and subsequent to hyperhomocysteinemia, which is associated with the formation of fibrinolysis-resistant blood thrombi.

No laughing matter - Myeloneuropathy due to heavy chronic nitrous oxide abuse.

 causing demyelination of the dorsal spinal columns, clinically indistinguishable from that which is caused by vitamin B12 deficiency.

[Extra hospital use of nitrous oxide for recreational purposes].

 and increases the blood levels of homocysteine and methylmalonyl CoA. The magnetic resonance of the spinal cord shows abnormalities in the majority of cases.

Lessons of the month: Nitrous oxide-induced functional vitamin B12 deficiency causing subacute combined degeneration of the spinal cord.

The patient reported heavy recreational use of

, which can cause functional deficiency of 

Nitrous oxide toxicity: When laughing gas is no laughing matter – A discussion of two cases

 are due to the irreversible inactivation of 

 which leads to decreased recycling of homocysteine to methionine thus preventing methylation of myelin proteins leading to demyelination in the central and peripheral nervous systems.

Recovery Following a Delayed Diagnosis of Subacute Combined Degeneration

His rapid progression to quadriparesis was attributed to

Subacute Combined Degeneration from Nitrous Oxide Abuse

 causes permanent oxidation of cobalt ions in 

 inhibiting this conversion and decreasing availability of functional vitamin B12, although measured vitamin B12 levels may not reflect this functional deficiency, particularly in adolescents.

Reply to: Comment on: Successful use of nitrous oxide during lumbar punctures: A call for nitrous oxide in pediatric oncology clinics

 concentration <200 pg/ml in normal children in the United States was exceedingly rare and seen in only 24 of 5,382 … in one-third of ALL patients from third-world countries due to malnourishment.7 This is a group of patients in whom 

Subacute combined degeneration of the spinal cord following nitrous oxide anesthesia: A systematic review of cases

 (N2O) is an anesthetic which oxidizes the cobalt ion of 

, interfering with its function as a coenzyme.

Nitrous oxide induced subacute combined degeneration with longitudinally extensive myelopathy with inverted V-sign on spinal MRI: a case report and literature review

), a long-standing anesthetic, is also neurotoxic by interfering with the bioavailability of 

Reply: Methotrexate neurotoxicity due to drug interactions: an inadequate folinic acid effect

 co-factor for methionine synthase rather than directly interfering with Methotrexate-induced inhibition of dihydrofolate reductase [8].

Smoking Discriminately Changes the Serum Active and Non-Active Forms of Vitamin B12.

The research proposed that organic nitrites,

, cyanides, and isocyanides of cigarette smoke interfere with 

 metabolism, and convert it to inactive forms.

When the Laughing Stops: Subacute Combined Spinal Cord Degeneration Caused by Laughing Gas Use.

An unusual cause of falls in a young woman.

 via oxidation, which can precipitate a demyelinating myelopathy akin to the classical B12 deficiency syndrome, subacute combined degeneration of the spinal cord.

Nitrous Oxide-induced Subacute Combined Degeneration Presenting with Dystonia and Pseudoathetosis: A Case Report.

The role of air pollution exposures in mediating nutritional biochemical profiles in autism: A reply to Jory (2015).

 irreversibly oxidizes the cobalt ion within 

, leaving vitamin B12 inactive and inducing neurologic impairment [2,3] through the inhibition of methionine synthase

 and targets the dynorphin/kappa opioid receptor system, and this particular subtype has been implicated in both feeding behavior and metabolic activities.

Recreational nitrous oxide use: Prevalence and risks.

, resulting in a functional vitamin B12 deficiency and initially causing numbness in fingers, which may further progress to peripheral neuropathy and megaloblastic anemia.

Whippits, nitrous oxide and the dangers of legal highs

 can have disabling neurological sequelae due to functional inactivation of 

Homocysteine levels and bad obstetric outcome among female operating room personnel occupationally exposed to nitrous oxide.

Notorious oxide.

 has an unusual pharmacologic side effect that is unrelated to its anesthetic action: it inactivates 

Nitrous Oxide Anesthesia and Plasma Homocysteine in Adolescents

, inhibits methionine synthase, and consequently increases plasma total homocysteine (tHcy).

Pre‐operative vitamin B infusion and prevention of nitrous oxide‐induced homocysteine increase

 with detrimental consequences for folate and methionine metabolism, detectable by an increase in total plasma homocysteine.

A common gene variant in methionine synthase reductase is not associated with peak homocysteine concentrations after nitrous oxide anesthesia

 leads to the inactivation of methionine synthase resulting in elevated plasma total homocysteine concentrations.

[Postoperative dementia: toxicity of nitrous oxide].

 cobalt's atom responsible for its inactivation and the appearance of clinical manifestations.

Avoidance of Nitrous Oxide for Patients Undergoing Major Surgery: A Randomized Controlled Trial

, folate metabolism, and deoxyribonucleic acid synthesis and prevents the use of high inspired oxygen concentrations, the consequences of these effects are unclear.

When nitrous oxide is no laughing matter: nitrous oxide and pediatric anesthesia

Although often felt to be relatively innocuous,

 can have significant metabolic effects in settings of abnormal 

 and B12‐related metabolism in children.

Adverse effect of nitrous oxide in a child with 5,10-methylenetetrahydrofolate reductase deficiency.

 irreversibly oxidizes the cobalt atom of 

, inhibiting the cobalamin-dependent enzyme methionine synthase, which has a key role in many biochemical reactions that involve the nervous system.

Nitrous oxide and vitamin B12

, the active derivative of vitamin B12 and essential cofactor for the transfer of the methyl group from …

Acute neurologic decompensation in an infant with cobalamin deficiency exposed to nitrous oxide.

 and may be a dangerous anesthetic in patients with cobalamin deficiency.

Nitrous oxide: time to stop laughing?

This confirmed the earlier work of Banks et al. [10] who showed that

 from the monovalent form to the bivalent form and thus inactivates it.

Cobalamin, the stomach, and aging.

Decisions about the optimal management of the very common problem of mild, preclinical cobalamin deficiency in … further clarification of the processes and the complex issues involved, including the possibility that routine

 use during surgery, proposed dietary changes, … practices may further stress the 

[Nitrous oxide exposure of operating room personnel in intubation anesthesia].

 and thus decreases DNA production by inactivation of methionine synthase.

[Nitrous oxide exposure to personnel in a recovery room with modern climate control].

Nitrous oxide: from frolics to a global concern in 150 years

The use of nitrous oxide for anaesthesia has also been questioned in the last decades, when it was discovered that

 did in fact influence the function of various organ systems and that it might be toxic due to its inhibition of 

Vitamin B12 supplements as protection against nitrous oxide inhalation.

 supplements can reverse some of the effects of chronic 

Metabolic evidence of cobalamin deficiency in bone marrow cells harvested for transplantation from donors given nitrous oxide

, but clinically apparent sequelae ensue in nondeficient individuals only when exposure is prolonged.

Effect of Nitrous Oxide on Folate and Vitamin B12 Metabolism in Patients

Although an occasional patient may prove highly susceptible to and develop signs of severe

 and folic acid deficiency after exposure to 

, our findings suggest that this is a rare event.

Effect of cobalamin inactivation on folate metabolism of leukemic cells.

 coenzyme of methionine synthetase, an essential enzyme in folate metabolism.

Megaloblastic anaemia, cobalamin, and folate.

Current work on the relations between these two coenzymes are discussed, particularly those that have emerged in studies using

Cobalamin inactivation decreases purine and methionine synthesis in cultured lymphoblasts.

We investigated cobalamin deficiency by treating cultured human lymphoblasts with N2O since

 inhibits methionine synthetase activity by inactivating 

Investigations into the effect of nitrous oxide anaesthesia on folate metabolism in patients receiving intensive care.

 and impairs DNA synthesis in bone marrow cells.

Role of S-adenosylmethionine in DNA synthesis and haemopoiesis.

) can produce neurological damage and megaloblastic change in the bone marrow due to inactivation of 

Toxicity of bone marrow in dentists exposed to nitrous oxide.

This study provides direct evidence that occupational exposure to

 activity resulting in measurable changes in bone marrow secondary to impaired synthesis of deoxyribonucleic acid.

Absence of Signs of Vitamin B12 ‐ Nitrous Oxide Interaction in Operating Theatre Personnel

Prevention of nitrous oxide-induced megaloblastic changes in bone marrow using folinic acid.

N2O and urine methylmalonic acid in man.

 dependent enzymes, methylmalonyl-CoA-mutase and methione synthetase, are depressed by 

Effect of nitrous oxide anaesthesia on homocystine excretion

, oxidizing Cob(I)alamin to the inactive Cob(III) alamin form.

FIRST AID FOR SNAKE BITE IN AUSTRALIA

 might interfere with the metabolism or action of 

, without altering the results of clinical biochemical tests used to detect vitamin B12 deficiency.

MYELONEUROPATHY AFTER PROLONGED EXPOSURE TO NITROUS OXIDE

The neurological picture is similar to that of subacute combined degeneration of the spinal cord, and it is possible that

Astrocyte activation following nitrous oxide exposure is related to oxidative stress and glutamate excitotoxicity

 is commonly used as an anesthetic agent and its exposure produces prolonged inactivation of 

Effect of nitrous oxide on nickel deprivation in rats

 and a subsequent decrease in the vitamin B12-dependent enzymes methionine synthase and methylmalonyl CoA mutase.

Enhanced therapeutic effect of methotrexate in experimental rat leukemia after inactivation of cobalamin (vitamin B12) by nitrous oxide

 interferes selectively with the coenzyme function of 

 and causes inactivation of methionine synthetase, with subsequent impairment of folate metabolism and reduction of cellular proliferation.

Aging, chronic administration of ethanol, and acute exposure to nitrous oxide: Effects on vitamin B12 and folate status in rats

 metabolism, we examined the combined influence of these parameters on vitamin B12/folate status in a rodent model.

Toxicity of methotrexate in rats preexposed to nitrous oxide.

This phenomenon may be attributed to the synergistic effects of

 coenzyme of methionine synthase, and MTX, which inhibits dihydrofolate reductase, on folate metabolism.

Methylation Deficiency Causes Vitamin B12‐Associated Neuropathy in the Pig

Impaired formylation and uptake of tetrahydrofolate by rat small gut following cobalamin inactivation.

Methionine synthetase activity declined after exposure to

Nitrous oxide and vitamin B12 deficiency interact adversely on rat growth.

A significant synergistic retardation of growth was seen in rats deprived of

Vitamin B12 neuropathy is not due to failure to methylate myelin basic protein

We have examined myelin basic protein in brains of rats in which

Effects of nitrous oxide on maternal and embryonic folate metabolism in rats.

 prosthetic group of methionine synthetase.

Synergistic deleterious effects of nitrous oxide exposure and vitamin B12 deficiency.

Betaine delays the onset of neurological impairment in nitrous oxide-induced vitamin B-12 deficiency in fruit bats.

 in vivo, results in neurological impairment leading to ataxia and death in the fruit bat Rousettus .

Increased urinary excretion of formiminoglutamic acid in nitrous-oxide-treated rats and its reduction by methionine.

 and inactivates methionine synthetase of which cobalamin is a co-enzyme.

Cobalamin (Vitamin B12) Analogs Are Absent in Plasma of Fruit Bats Exposed to Nitrous Oxide 1

Cobalamin (vitamin B12) analogs were not detected in the plasma of fruit bats treated with

Cobalamin inactivation by nitrous oxide produces severe neurological impairment in fruit bats : protection by methionine and aggravation by folates.

 when administered to fruit bats, results in severe neurological impairment leading to ataxia, paralysis and death.

Urinary folate loss following inactivation of vitamin B12 by nitrous oxide in rats

Changes in tissue folates accompanying nitrous oxide-induced inactivation of vitamin B12 in the rat.

 and thus inactivates methionine synthetase which requires cobalamin as a coenzyme.

Recovery of tissue folates after inactivation of cobalamin by nitrous oxide. The significance of dietary folate.

 (N2O), oxidizes the cobalt moiety in the 

 molecule and in this way inactivates methionine synthetase which requires reduced cobalamin.

Inactivation of methionine synthase by nitrous oxide.

 promises to be a valuable tool in the study of vitamin B12 metabolism.

The effect of vitamin B12 inhibition in vivo: impaired folate polyglutamate biosynthesis indicating that 5-methyltetrahydropteroylglutamate is not its usual substrate.

Abstract Using 5-[14C] methyltetrahydropteroylglutamate and [3H] pteroylglutamate it was found that

 dependent methyltransferase can be inhibited in vivo in mice by 

A rise in cases of nitrous oxide abuse: neurological complications and biological findings

Nitrous oxide‐induced neurotoxicity: A case report and literature review

, which is an important co-factor in metabolic pathways involved in DNA and myelin synthesis.

, which is an important co‐factor in metabolic pathways involved in DNA and myelin synthesis.

Nitrous oxide and vitamin B12 in sickle cell disease: Not a laughing situation

 prolonged and recurrent administration is known to affect 

 metabolism with subsequent clinical consequences.

Neurological Manifestations of Myeloneuropathy in Patients with Nitrous Oxide Intoxication

) is a long-standing anesthetic that also exhibits neurotoxicity by interfering with the bioavailability of 

Unhappy End of ‘Happy Balloons’: Subacute Combined Degeneration Caused by Nitrous Oxide Gas

It is the well-documented complication of cobalamin (vitamin B12) deficiency, which is often observed … from pernicious anemia, various conditions leading to malnutrition, tropical sprue, or HIV infection.1

 (N2O) exerts neurotoxic … the bioavailability of 

, but N2O as an etiology of … well known and often underestimated.

Complications caused by nitrous oxide in dental sedation

 can lead to the irreversible inactivation of 

, which is essential for humans; although rare, this can be fatal in some patients.

Recreational Nitrous Oxide Abuse Causing Ischemic Stroke in a Young Patient: A Rare Case Report

 use can also lead to hyperhomocysteinemia by irreversibly oxidizing the cobalt atom of 

, which results in an inhibition of the enzyme methionine synthase.

Funicular Myelosis in a Butcher: It Was the Cream Cans

 uptake could not compensate the noxious effects of 

Copper control of bacterial nitrous oxide emission and its impact on vitamin B12-dependent metabolism

This cytotoxic N2O emission subsequently modulates expression of genes controlled by vitamin B12 riboswitches, because

Induction of Apoptosis in neoplastic cells by depletion of vitamin B12

 we show that, in a variety of cell lines in vitro, methionine synthase is rapidly inhibited, the cells cease proliferation and undergo apoptosis.

Nitrous oxide inactivation of cobalamin-dependent methionine synthase from Escherichia coli: characterization of the damage to the enzyme and prosthetic group.

, and here we characterize the modifications that occur to the Escherichia coli enzyme following electrochemical inactivation.

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Possible Interaction: Nitrous Oxide and Vitamin B 12

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Nitrous Oxide

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Research Papers that Mention the Interaction