The Use of Intraoperative Nitrous Oxide Leads to Postoperative Increases in Plasma Homocysteine

 inhibits methionine synthase, which aids in the conversion of homocysteine to 

Relationship among homocyst(e)ine, vitamin B-12 and cardiac disease in the elderly: association between vitamin B-12 deficiency and decreased left ventricular ejection fraction.

In vitro studies on rat heart revealed that

Myelotoxic, neurotoxic and reproductive adverse effects of nitrous oxide.

 have been shown to protect against megaloblastosis and neurotoxicity occurring following 

Massive hyperhomocysteinaemia as a complication of nitrous oxide inhalation

 synthetase and thus potentially leads to mild hyperhomocysteinaemia (<40 μmol l) with uncertain clinical significance when used as an anaesthetic agent for less than 3 h [3, 4].

Nitrous oxide and cardiovascular outcome: perspective from the POISE trial.

By irreversible oxidation of vitamin B12,

 effectively impairs conversion of homocysteine to 

, and consequently this impairment leads to dose-dependent plasma homocysteine Nitrous Oxide and Cardiovascular Outcome: Perspective from the POISE Trial

The enigma of ENIGMA-I.

 synthetase, which mediates an increase in homocysteine.

Anesthetic management of a parturient with hyperhomocysteinemia.

Neuraxial anesthesia techniques may be relatively contraindicated in anticoagulated patients, and

 may exacerbate the condition by inhibiting the conversion of homocysteine to 

Detection of inadvertent tracheal placement of nasogastric tubes

Effect of nitrous oxide on plasma homocysteine and folate in patients undergoing major surgery.

 synthetase resulting in elevated plasma homocysteine (Hcy) concentration after surgery.

Severe anaphylaxis during general anaesthesia in a β‐blocked cardiac patient: considerations

N2O anesthesia may exacerbate hyperhomocysteinemia and endothelial dysfunction in patients with renal impairment.

 directly inhibits methionine synthase, which contains cobalamin as a prosthetic group and catalyzes a folate-dependent conversion of homocysteine to 

The above-mentioned catastrophic events may provide us a cautionary message; plasma homocysteine and

 levels should be closely monitored in patients with renal impairment undergoing 

[The effect of midazolam on the memory during cesarean section and the modulation by flumazenil].

 could produce retrograde amnesia, when combined with 

Effect of Methionine and Nitrous Oxide on Homocysteine Export and Remethylation in Fibroblasts from Cystathionine Synthase-Deficient, cblG, and cblE Patients

, so that in the presence of nitrous oxide, the Hey export became less dependent of methionine.

Preoperative Methionine Loading Enhances Restoration of the Cobalamin‐dependent Enzyme Methionine Synthase after Nitrous Oxide Anesthesia

Furthermore, preoperative administration of

 should be considered as a means to counteract adverse effects of 

Effect of cobalamin inactivation on folate metabolism of leukemic cells.

 synthetase, an essential enzyme in folate metabolism.

Adenosine dialdehyde and nitrous oxide induce HL-60 differentiation.

The differentiation induced by adenosine dialdehyde was prevented by homocysteine and that by

Nitrous oxide during pregnancy

COBALAMIN INACTIVATION DECREASES PURINE AND METHIONINE SYNTHESIS IN CULTURED HUMAN LYMPHOBLASTS: 22

 synthetase activity by inactivating cobalamin, cultured lymphoblasts were treated with N2O to create a model of cobalamin deficiency; 4 h of N2O exposure reduced rates of methionine synthesis by 89%.

Cobalamin inactivation decreases purine and methionine synthesis in cultured lymphoblasts.

Role of S-adenosylmethionine in DNA synthesis and haemopoiesis.

, in the form of S-adenosylmethionine (SAM), being required for DNA synthesis and the prevention of the development of megaloblastic anaemia in man.

Altered vitamin B12 metabolism in fibroblasts from a patient with megaloblastic anemia and homocystinuria due to a new defect in methionine biosynthesis.

Exposure of control fibroblasts during culture, but not of fibroblasts from this patient, to

 significantly reduced the holoenzyme activity of 

N2O and urine methylmalonic acid in man.

These findings indicate that the 2 vitamin B-12 dependent enzymes, methylmalonyl-CoA-mutase and

Effect of nitrous oxide anaesthesia on homocystine excretion

 depresses the two known vitamin B12 dependent enzymes methylmalonyl CoA mutase and 

 synthetase by inactivation of their coenzymes adenosylcobalamin and methylcobalamin respectively.

Nitrous Oxide Inactivates Methionine Synthetase in Human Liver

 synthetase progressively increased as the product of the concentration of 

Effect of nitrous oxide on human bone marrow cells and its synergistic effect with methionine and methotrexate on functional folate deficiency.

 or methotrexate have a synergistic effect on depletion of functional folate, N2O alone or in combination with methionine or methotrexate might be of value for cancer treatment and deserve clinical trials.

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 vitamin B12 and causes inactivation of 

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

Effect of low and high doses of nitrous oxide on preproenkephalin mRNA and its peptide methionine enkephalin levels in the hypothalamus

 enkephalin was significantly higher after 24 and 48 h of exposure of 

 than after exposure to 12 h of N2O or air.

Effect of nitrous oxide on haematopoiesis in vitro: biochemical and functional features.

In haematopoietic and bone marrow stromal cells,

 synthetase activity with a corresponding increase in homocysteine efflux.

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

 synthase activities in liver, kidney and brain, and recovery of methionine synthase activities occurred over a period of 4 days in both the aged ethanol-fed and control groups.

Effect of nitrous oxide and methionine on hepatic S-adenosylmethionine levels and in vivo histidine oxidation in rats.

 greatly increased hepatic levels of AdoMet and increased histidine oxidation in normal and 

Vitamin B12 and folate status in rats after chronic administration of ethanol and acute exposure to nitrous oxide.

 synthase activities, and recovery of methionine synthase activity after N2O occurred over a period of 4 days at the same rate in both the ethanol-fed and control groups.

Short term effect of nitrous oxide on methionine and S-adenosyl methionine concentrations.

Hepatic SAM was unchanged, but there was a highly significant reduction in

, to 62% of control, after 80 min exposure to 

Nitrous oxide induced vitamin B12 deficiency: measurement of methylation reactions in the fruit bat (Rousettus aegyptiacus).

 synthetase activity has been proposed as a suitable model for the myelopathy associated with vitamin B12 deficiency.

The Influence of Nitrous Oxide on Methionine, S‐adenosylmethionine, and Other Amino Acids

 can decrease the concentrations of two intermediary metabolites (

 and S-adenosylmethionine) that are important in the control of methylation reactions and in the maintenance of the active form of tetrahydrofolic acid.

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

 oxidizes the vitamin B12 prosthetic group of 

Folate polyglutamate synthetase activity in the cobalamin-inactivated rat.

 inactivates cob[I]alamin and interferes with the activity of 

 synthetase, of which cob[I]alamin is a coenzyme.

Nitrous Oxide Does Not Hinder the Repair of Halothane‐Induced Hepatic Injury in the Rat

 administration may limit DNA synthesis by inactivating 

 synthetase, and may thus hamper the repair of an injured organ such as the liver.

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

A significant decrease is produced, while on

 synthetase of which cobalamin is a co-enzyme.

Methanol toxicity in the monkey: effects of nitrous oxide and methionine.

Treatment of nitrous oxide-exposed … with repetitive doses of

 (100 mg/kg 10, 12 and 14 … after methanol) reversed the effects of 

 on formate oxidation, resulting in a marked decrease in blood formate levels and an increase in the rate of [14C]O2 formation from methanol.

The role of methionine in the intracellular accumulation and function of folates.

The vital role of the methylation reactions was demonstrated by exposing monkeys to

The regulation of one-carbon oxidation in the rat by nitrous oxide and methionine.

 synthetase activity, reduced hepatic S-adenosyl- l -methionine (Ado-Met) and tetrahydrofolate (H4 folate) concentrations and decreased the rate of formate oxidation in the rat.

Inactivation of Methionine Synthetase by Nitrous Oxide in Mice

 (approximately 1100 ppm) for eight to 22 days produced a small but significant reduction in liver and 

 exhibited more than a 50 per cent decrease in 

 synthetase activity within 30 min, and activity dropped to 5–25 per cent of the original value after a 4-hour exposure.

VITAMIN B12 REGULATES FOLATE METABOLISM BY THE SUPPLY OF FORMATE

 (N2O) inactivates the B12 coenzyme involved in 

 synthesis and interrupts formation of the folate coenzyme (folate polyglutamate).

SELECTIVE INACTIVATION OF VITAMIN B12 IN RATS BY NITROUS OXIDE

 rapidly inactivated the cytosol enzyme, 

 synthetase, but the mitochondrial enzyme, methylmalonyl CoA mutase, seemed to be unaffected, although both enzymes require vitamin B12.

Evaluation of total greenhouse gas emissions during sewage sludge composting by the different dicyandiamide added forms: Mixing, surface broadcasting, and their combination.

 and M+B treatments significantly decreased by 35.1% and 51.8%, respectively.

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Possible Interaction: Methionine and Nitrous Oxide

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Research Papers that Mention the Interaction