scholarly journals Influence of Vitamin B12 Status on the Inactivation of Methionine Synthase by Nitrous Oxide

1993 ◽  
Vol 37 (2) ◽  
pp. 63
Author(s):  
M. J. LANDON ◽  
P. CREAGH-BARRY ◽  
S. McARTHUR ◽  
A. CHARLETT
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Methionine Synthase

scholarly journals INFLUENCE OF VITAMIN B12 STATUS ON THE INACTIVATION OF METHIONINE SYNTHASE BY NITROUS OXIDE

1992 ◽  
Vol 69 (1) ◽  
pp. 81-86 ◽  
Author(s):  
M.J. LANDON ◽  
P. CREAGH-BARRY ◽  
SARA McARTHUR ◽  
A. CHARLETT
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Methionine Synthase

scholarly journals In vitro inactivation of methionine synthase by nitrous oxide.

1986 ◽  
Vol 261 (34) ◽  
pp. 15823-15826
Author(s):  
V Frasca ◽  
B S Riazzi ◽  
R G Matthews
Keyword(s):  
Nitrous Oxide ◽  
Methionine Synthase

Association of homocysteine (but not of MTHFR 677 C>T, MTR 2756 A>G, MTRR 66 A>G and TCN2 776 C>G) with ischaemic cerebrovascular disease in Sicily

2006 ◽  
Vol 96 (08) ◽  
pp. 154-159 ◽  
Author(s):  
Rosa-Maria Guéant-Rodriguez ◽  
Guido Anello ◽  
Rosario Spada ◽  
Antonino Romano ◽  
Adrian Fajardo ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Vitamin B12 ◽  
Methylenetetrahydrofolate Reductase ◽  
Methionine Synthase ◽  
Italian Population ◽  
Significant Independent Predictor ◽  
Methionine Synthase Reductase ◽  
Ischaemic Cerebrovascular Disease ◽  
Folate And Vitamin B12 ◽  
Neutral Effect

SummaryAssociation between methylenetetrahydrofolate reductase polymorphism (MTHFR 677 C>T), a determinant of homocysteine plasma level (t-Hcys), with ischaemc cerebrovascular disease (iCVD) seems to be neutral in North Europe and North America. The association of 2756 A>G of methionine synthase (MTR), 66 A>G of methionine synthase reductase (MTRR) and 776 C>G of transcobalamin (TCN2) needs to be evaluated further. It was the objective of this study to evaluate the association of these polymorphisms, t-Hcys, vitamin B12 and folate levels with iCVD, in an Italian population from Sicily. We investigated the association of these polymorphisms, t-Hcys, vitamin B12 and folate with iCVD in 252 subjects, including 131 cases and 121 sexand agematched healthy controls. t-Hcys was higher in the iCVD group than in controls [15.3 (11.5–17.9) vs. 11.6 (9.4–14.5) µM; P=0. 0007] and also in subjects withTCN2 776CG genotype, compared to homozygous genotypes [13.5 (9.9± 16.9) vs. 11.7 (9.6 ± 14.4) µM; P=0. 0327]. The folate level in cases and controls was consistent with an adequate dietary intake [12.7 (9.0–15.3) vs. 12.5 (9.6–16.9) nM; P=0. 7203]. In multivariate analysis, t-Hcys was a significant independent predictor of iCVD with an odds ratio of 1.14 (95% C.I. : 1.06–1.24; P=0. 0006). No association was found between MTHFR, MTR, MTRR and TCN2 polymorphisms and iCVD risk. We have found an influence of t-Hcys and a neutral effect of MTHFR, MTR, MTRR and TCN2 on iCVD risk in Sicily. The neutral influence of these polymorphisms may be explained by adequate status in folate and vitamin B12. Other factors underlying the increased t-Hcys need further investigations.

scholarly journals The effects of nitrous oxide on vitamin B12 and homocysteine levels in methyltetrahydrofolate reductase gene mutation

2013 ◽  
Vol 114 (06) ◽  
pp. 317-322 ◽  
Author(s):  
S. Hakimoglu ◽  
V. Hanci ◽  
Y. Hakimoglu ◽  
S. Cicek ◽  
S. Yurtlu ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Gene Mutation ◽  
Reductase Gene ◽  
Methyltetrahydrofolate Reductase

scholarly journals Vitamin B12-responsive neonatal megaloblastic anemia and homocystinuria with associated reduced methionine synthase activity

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1128-1133 ◽  
Author(s):  
LJ Hallam ◽  
M Sawyer ◽  
AC Clark ◽  
MB Van der Weyden
Keyword(s):  
Vitamin B12 ◽  
Developmental Delay ◽  
Genetic Heterogeneity ◽  
Megaloblastic Anemia ◽  
Methylmalonic Aciduria ◽  
Methionine Synthase ◽  
Cultured Fibroblasts ◽  
Neurologic Recovery ◽  
Neurologic Development ◽  
Growth Requirement

Abstract We present findings on an infant with neonatal megaloblastic anemia, homocystinuria, and neurologic dysfunction that included developmental delay and tonic seizures. There was no methylmalonic aciduria. Cyanocobalamin therapy was accompanied by complete hematologic and neurologic recovery, diminished homocystine excretion, and subsequently normal neurologic development. Cultured fibroblasts and lymphoblasts showed a reduced methionine synthase activity and a growth requirement for methionine. Cobalamin incorporation by the patient's lymphoblasts was normal, but the proportion of cellular methylcobalamin in the patient's lymphoblasts and fibroblasts were markedly reduced and that of adenosylcobalamin normal. The reduced methionine synthase activity was independent of assay reducing (thiol) conditions, but normal levels of activity accompanied culture of the patient's lymphoblasts in medium with markedly increased cobalamin concentration. The characteristics of the reduced methionine synthase of our patient differ significantly from that of the previously described infant with cobalamin E disease and suggest that genetic heterogeneity may characterize this mutation.

Alterations in mammalian cells induced by inactivation of vitamin B12 with nitrous oxide

Vitamin B12 ◽  
1979 ◽  
pp. 1061-1064 ◽  
Author(s):  
B. Reed ◽  
J. Dinn ◽  
S. McCann ◽  
P. Wilson ◽  
H. O’Sullivan ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Mammalian Cells

scholarly journals An Acute, Severe Axonal Sensorimotor Polyneuropathy in the Setting of Nitrous Oxide Abuse

2020 ◽  
Vol 10 (4) ◽  
pp. 293-296
Author(s):  
Jules C. Beal ◽  
Yishan Cheng ◽  
Sabiha Merchant ◽  
Reza Zarnegar
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Clinical Picture ◽  
Guillain Barre Syndrome ◽  
Sensory Loss ◽  
Laboratory Evaluation ◽  
Sensorimotor Polyneuropathy ◽  
Guillain Barré Syndrome ◽  
B12 Deficiency ◽  
Guillain Barré

Nitrous oxide, often used as an anesthetic agent, is also increasingly a drug of abuse due to its euphoric and anxiolytic effects. Frequent exposure to nitrous oxide can lead to neurologic complications, including B12 deficiency and resultant subacute myeloneuropathy, as well as direct neurotoxicity. A clinical presentation of acute sensorimotor polyneuropathy mimicking Guillain-Barré syndrome after chronic nitrous oxide abuse has been reported only rarely. Here we present a 17-year-old previously healthy girl presented with 10 days of progressive ascending sensory loss and weakness in the legs. She admitted to heavy nitrous oxide abuse over a period of a year or more. Laboratory evaluation was significant for normal vitamin B12 level with elevated homocysteine. A magnetic resonance imaging (MRI) of her spine showed abnormal signal involving the bilateral dorsal columns. Nerve conduction studies were suggestive of severe axonal sensorimotor polyneuropathy. This patient demonstrates concurrent multifactorial neurologic injury as a result of nitrous oxide abuse. She had a functional vitamin B12 deficiency as indicated by the elevated homocysteine, leading to a subacute combined degeneration that was evident on the MRI. In addition, she had evidence of direct neurotoxicity leading to axonal injury and sensorimotor polyneuropathy reminiscent of Guillain-Barré syndrome. This clinical picture is a serious but seldom reported possible complication if nitrous oxide abuse and should be considered in patients presenting with a clinical picture suspicious for Guillain-Barré syndrome or its variants.

scholarly journals 118 Case series: subacute combined degeneration of the spinal cord in vitamin B12-replete recreational nitrous oxide abusers

2019 ◽  
Vol 90 (e7) ◽  
pp. A38.2-A39
Author(s):  
Chris Blair ◽  
Chris Tremonti ◽  
Leon Edwards ◽  
Paul Haber ◽  
Michael Halmagyi
Keyword(s):  
Nitrous Oxide ◽  
Vitamin B12 ◽  
Prolonged Exposure ◽  
Serum Vitamin ◽  
Case Series ◽  
The Body ◽  
Enzymatic Reactions ◽  
Full Time ◽  
Central Demyelination ◽  
Vitamin B12 Supplementation

IntroductionWithin a few years of its discovery in late 18th century, nitrous oxide was being used recreationally for its pleasurable effects. It remains in widespread use as an inhaled stimulant today, and can be legally acquired in bulk quantities with relative ease. In the body prolonged exposure to nitrous oxide leads to the oxidization of vitamin B12, rendering it unusable in key enzymatic reactions necessary for myelin synthesis. Over time this qualitative deficiency leads to a central demyelination syndrome that characteristically develops despite normal serum vitamin B12 levels and, with continued exposure to nitrous oxide, resists treatment with vitamin B12 supplementation.MethodNitrous oxide abusers presenting with a central demyelination syndrome were enrolled in this case series. Serum levels of vitamin B12, active B12, folate and homocysteine were measured. Nitrous oxide exposure was discontinued, and all patients were treated in accordance with evidence-based guidelines.ResultsEight patients presented with predominantly moderate-to-severe clinical deficits. The majority were vitamin B12 replete. In most cases individuals had actively engaged in prolonged vitamin B12 supplementation in an attempt to circumvent the harmful pathophysiology, of which they were loosely aware. Following treatment and rehabilitation several patients were discharged into full-time care, and most had significant residual disability at follow-up.ConclusionsThis case series not only illustrates the tragic consequences of abuse of this widely available and legally procured stimulant, but also highlights the futility of pursuing a nominally ‘protective’ strategy of vitamin B12 supplementation in the context of continued nitrous oxide exposure.

scholarly journals Stimulation in vitro of vitamin B12-dependent methionine synthase by polyamines

1996 ◽  
Vol 316 (2) ◽  
pp. 661-665 ◽  
Author(s):  
Susan H. KENYON ◽  
Anna NICOLAOU ◽  
Tamara AST ◽  
William A. GIBBONS
Keyword(s):  
Enzyme Activity ◽  
Vitamin B12 ◽  
Cell Signalling ◽  
Methionine Synthase ◽  
Polyamine Metabolism ◽  
Physiological Concentration ◽  
Methylation Pathway ◽  
Important Enzyme

Vitamin B12-dependent methionine synthase is an important enzyme for sulphur amino acid, folate polyamine metabolism, S-adenosylmethionine metabolism and also in the methylation pathway of DNA, RNA, proteins and lipids. Consequently, studies aiming at exploring the control and regulation of methionine synthase are of particular interest. Here we report the modulation of enzyme activity in vitro by polyamines. Although putrescine, cadaverine, spermine and spermidine all stimulated enzyme activity, the last two were the most potent, causing increases in enzyme activity up to 400%. The EC50 for spermine was determined as 8 μM and for spermidine 40 μM. The physiological concentration for spermine has been reported to be 15–19 μM. Spermine was found to increase both the Km and the Vmax with respect to methyltetrahydrofolate for the enzyme. These data support the hypothesis that spermine and spermidine are feedback regulators of methionine synthase both in vivo and in vitro and are consistent with the polyamines' regulating cell signalling pathways.

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