Why this poison is interesting

Every other poison in this library does something a pharmacologist would recognise: it binds a receptor, blocks a channel, saturates an enzyme, or is converted into something that does. Nitrous oxide performs a redox reaction on a metal atom. It oxidises the cobalt ion at the centre of vitamin B12³ — from the monovalent Co(I) state to Co(III), which is textbook cobalamin chemistry rather than a figure quoted from the review — and in doing so ends the catalytic life of that molecule of cobalamin. Nothing is metabolised. Nothing accumulates. The gas leaves in the breath within minutes and the damage it has already done stays behind.

The second reason is the timescale. This site's signature component draws a latent phase as a visible gap between what you see and what is happening. Nitrous oxide's gap is measured in weeks, and in the meantime the user experiences a drug with an unusually benign acute profile: brief, cheap, legal to possess until recently, sold in catering canisters, and followed by no hangover. The mechanism is entirely silent until enough cobalamin has been inactivated, and by then the injury is to myelin.

The third is diagnostic. The serum vitamin B12 concentration is frequently normal, because the vitamin is still there — it is simply no longer able to work. A clinician who orders a B12 level, finds it within range and excludes the diagnosis has been defeated by the mechanism. The informative tests are the substrates that accumulate upstream of the blocked reactions: homocysteine, and methylmalonic acid.³

A poison is a drug whose kinetics have escaped its pharmacology.

The toxic principle

Vitamin B12 is a corrin ring with a cobalt ion at its centre. That cobalt cycles through three oxidation states during catalysis, and the chemistry of the whole vitamin depends on its ability to reach the highly reduced Co(I) state, which is one of the most powerful biological nucleophiles known. Nitrous oxide oxidises it, and an oxidised cobalamin cannot complete the catalytic cycle.

Methionine synthase performs a single reaction that sits at the junction of two cycles. It takes a methyl group from 5-methyltetrahydrofolate and transfers it, via the cobalt of methylcobalamin, onto homocysteine to make methionine. Stop that reaction and three things happen at once: homocysteine accumulates behind the block, methionine is not made, and folate is trapped in its methylated form and cannot be recycled into the pool needed for DNA synthesis.

Methionine is not merely an amino acid. It is the precursor of S-adenosylmethionine, the universal methyl donor for the cell — for DNA, for RNA, for proteins, and for the lipids and basic proteins of myelin. A cell that cannot make methionine cannot methylate anything. That is the step at which a redox reaction on a trace metal becomes a neurological disease.

The step that is taught more confidently than it is known

The standard teaching runs: methionine synthase stops, methionine falls, methylation of myelin fails, the cord demyelinates. Gernez and colleagues measured plasma methionine in 93 patients who chronically consumed nitrous oxide, stratified into four groups by a Peripheral Neuropathy Disability score. Methionine did correlate inversely with clinical severity (Spearman −0.42, p < 10⁻⁵), and inversely with homocysteine (−0.57, p < 10⁻⁹) — confirming the action on methionine synthase. But the average methionine level in all four groups lay within the physiological range (16–23 µmol/L), and the authors conclude that a decrease in plasma methionine cannot be imputed as the only mechanism involved in the pathophysiology, and that other mechanisms probably need to be identified.⁴ The enzyme block is established; the simple methionine-deficiency explanation for the myelopathy is not. Traditional teaching

What else might be going on is an active question rather than a settled alternative. The mechanistic review by Joncquel Chevalier-Curt and colleagues reframes the problem as a pathology of methylation in general — DNA, RNA and protein — and points specifically at protein arginine methyltransferases involved in myelinogenesis, alongside disruption of the folate cycle, the transsulfuration pathway, glutathione synthesis and the fuelling of the Krebs cycle by methylmalonyl-CoA.³ That is a wider lesion than a single missing amino acid, and it fits a disease that damages myelin in a specific anatomical pattern rather than damaging cells generally.

Toxicokinetics

The kinetics table below is unusual because almost every row argues that the kinetics do not matter. Nitrous oxide is insoluble, unmetabolised and gone within minutes. The parameter that governs the disease is not a plasma concentration but a cumulative number of canisters, and there is no assay for that.

Nitrous oxide — kinetics that predict nothing about the injury
Parameter	Therapeutic	In overdose	Why it changes
Absorption	Inhaled; alveolar uptake is essentially instantaneous	Same. Effect within seconds of a breath from a balloon	The onset is limited by circulation time, not by absorption. This is why the recreational pattern is dozens of short exposures rather than one long one — and why the dose is counted in canisters.
Blood–gas partition coefficient	Very low (about 0.47) — nitrous oxide is poorly soluble in blood	Unchanged	Low solubility means rapid equilibration in both directions. The reason it wears off in minutes is the same reason it works in seconds, and it is why the acute effect gives no warning of the chronic one.
Distribution	Distributes to all perfused tissue; enters air-filled spaces and expands them	Unchanged	The expansion into gas-containing spaces is an anaesthetic consideration rather than a toxicological one, but it is the mechanism behind the barotrauma occasionally reported after very heavy use.
Metabolism	None of consequence. Nitrous oxide is not biotransformed by human enzymes	None	This is the row that separates nitrous oxide from every other page in this library. There is no bioactivation and no toxic metabolite. The gas is chemically reactive enough to do its damage unaided, on contact with a reduced cobalt ion.
Elimination	Exhaled unchanged, within minutes of the last breath	Unchanged	Elimination is complete and fast, and it is irrelevant to the outcome. The gas has gone; the inactivated cobalamin has not. Nothing about clearance predicts recovery.
The injury's real dose axis	—	Cumulative exposure over weeks to months, not concentration at a moment	There is no plasma level to measure and no threshold to quote. The measurable consequences are the substrates that pile up behind the two blocked enzymes: homocysteine and methylmalonic acid.³
Serum vitamin B12	—	Frequently normal, because the vitamin is present but inactivated	The single most important line in this table. A normal B12 does not exclude functional B12 deficiency caused by nitrous oxide: the enzyme block is upstream of the assay, which measures the molecule and not its oxidation state. That inference is this page's own, drawn from the mechanism — it is not a quoted finding. What the cited review does support is the other half: homocysteine measurements obviously help diagnosis, with methylmalonate among the additional markers.³
Dialysability	—	Not applicable, and never assessed. EXTRIP has published no recommendation covering nitrous oxide⁵	A gas that leaves in the breath within minutes cannot be a target for extracorporeal removal, and the patient presents weeks after the exposure that mattered. This is one of a small group of entries where the absence of an EXTRIP recommendation reflects a question not worth asking — cyanide, hydrogen sulphide and the asphyxiant gases are the others, rather than one merely unasked.

Metabolism and the metabolites

There are none. That sentence is the section, and it is worth pausing on: this is the only page in the library where the metabolism section describes the metabolism of something other than the poison. What follows is the metabolism nitrous oxide interrupts.

What nitrous oxide breaks — the methionine synthase reaction and everything downstream

Nitrous oxideUnmetabolised. Reacts directly with the cobalt ion of cobalamin³
Inactivated cobalaminThe vitamin is still present and still measurable — it can no longer complete the catalytic cycle³
Methylcobalamin lost — enzyme inactivatedMethionine synthase stopsThe principal lesion. Homocysteine + 5-methyl-THF → methionine no longer proceeds³
Adenosylcobalamin depletedMethylmalonyl-CoA mutase starvedMethylmalonic acid accumulates³ — the second diagnostic marker, and a separate failure mode from the first
Raised plasma homocysteineThe most useful single test.³ Inversely correlated with methionine in 93 users (Spearman −0.57, p < 10⁻⁹)⁴
S-adenosylmethionine fallsThe universal methyl donor. Methylation of DNA, RNA, protein and myelin lipid all depend on it³
Functional folate deficiencyThe folate trap — why the marrow picture of B12 deficiency and of folate deficiency are indistinguishable
Demyelination of the dorsal and lateral columnsThe clinical endpoint¹ — though the step from failed methylation to this specific anatomy is where the evidence thins⁴

Two of the earliest demonstrations still frame the field. Deacon and colleagues showed in 1978 that nitrous oxide selectively inactivates vitamin B12 in rats² — the animal counterpart of the human chemistry, though selective there means selective between the two enzymes: they found methionine synthetase rapidly inactivated and methylmalonyl-CoA mutase apparently unaffected.² The dual-enzyme account above rests on the later review³ and on human methylmalonic acid data, not on Deacon. In the same year, Layzer described the human syndrome: 15 patients, all but one of them dentists — 13 of whom had abused the gas for periods from three months to several years, while two were exposed occupationally alone, in poorly ventilated surgeries — with Lhermitte's sign, gait ataxia, leg weakness, sphincter disturbance and a sensorimotor polyneuropathy, in a picture he described as similar to that of subacute combined degeneration of the spinal cord.¹ Layzer went no further than to suggest it is possible that nitrous oxide interferes with the action of vitamin B12 in the nervous system¹ — a caution the intervening five decades have justified in outline and complicated in detail.

Elimination and accumulation

Nitrous oxide does not accumulate. The damage accumulates. That inversion is the whole clinical problem, and it defeats the intuition every clinician builds from every other poisoning: that the drug goes away and the patient gets better.

Background vitamin B12 status is a genuine modifier of susceptibility rather than a footnote. Somebody whose cobalamin stores are already marginal — a vegan diet without supplementation, pernicious anaemia, previous bariatric surgery, metformin use, or simply nutritional depletion in the context of heavy drug use — has less reserve for the gas to consume. This is the closest the page comes to a risk-stratification statement, and it belongs to clinical assessment rather than to a number.

Target organs — and why those

Every cell in the body uses methionine synthase, and only a few tissues declare a failure of it. The selectivity is the mechanism, and it is the reason this page has an organ section at all.

Spinal cord — dorsal and lateral columns

TargetMyelin of the posterior columns and corticospinal tracts

Why hereThe classical anatomy of subacute combined degeneration, reproduced by the gas. Why these tracts and not others is the least satisfying answer on this page. The conventional account invokes the long, heavily myelinated axons' exceptional demand for methylation-dependent myelin maintenance — but Gernez's data show methionine within the physiological range even in severely affected users, and the authors state explicitly that methionine deficiency cannot be the only mechanism.⁴ Joncquel Chevalier-Curt's review proposes a broader methylation failure, including protein arginine methyltransferases involved in myelinogenesis.³ The anatomy is established; the reason for it is not. Traditional teaching

At the bedsideLhermitte's sign, loss of vibration and joint position sense, sensory ataxia with a positive Romberg, spastic paraparesis and brisk reflexes with extensor plantars — the combined picture of dorsal-column and pyramidal involvement.¹ MRI may show a T2-hyperintense signal in the posterior cord, often over several segments.

Peripheral nerves

TargetLarge myelinated sensory and motor axons

Why hereLayzer's electrodiagnostic studies pointed to an axonal polyneuropathy rather than a purely demyelinating one¹, which is a genuinely awkward finding for a story built entirely on myelin. It suggests the metabolic lesion reaches the axon itself, plausibly through the same failure of methylation-dependent maintenance, and it is one reason the simple account is incomplete. Inferred

At the bedsideDistal paraesthesiae and numbness, usually the first symptom and often dismissed. Combined with cord involvement it produces the confusing examination of absent ankle reflexes with extensor plantars.

Bone marrow

TargetDNA synthesis in erythroid precursors

Why hereA folate problem rather than a myelin one. With methionine synthase blocked, folate is trapped as 5-methyltetrahydrofolate and cannot be recycled into the tetrahydrofolate pool needed for thymidylate synthesis, so nuclear maturation lags behind cytoplasmic maturation in the fastest-dividing cells. This is the same final common path as dietary folate deficiency, which is why the film cannot distinguish them. Established

At the bedsideMacrocytosis, hypersegmented neutrophils, occasionally frank megaloblastic anaemia. Its absence does not exclude the diagnosis — the neurology can precede or occur without any haematological change.

Vascular endothelium

TargetConsequences of accumulated homocysteine

Why hereHomocysteine rises because it sits immediately behind the blocked reaction, and hyperhomocysteinaemia is associated with thrombosis. The association is well established in inherited homocystinuria; attributing an individual thrombotic event in a nitrous oxide user to the homocysteine specifically is an inference from that association, not a demonstrated causal chain in this population. Inferred

At the bedsideCase reports describe venous and arterial thrombotic events in heavy users. Homocysteine is measured here primarily as a diagnostic marker of the enzyme block³, and its prognostic meaning for vascular risk in this setting is not established.

Brain

TargetWidespread methylation-dependent processes; NMDA receptor antagonism acutely

Why hereTwo entirely separate effects share this organ and should not be confused. The acute euphoria and dissociation are receptor pharmacology — nitrous oxide is an NMDA receptor antagonist, which is what it shares with ketamine — and reverse completely within minutes. The chronic effects follow the cobalamin lesion. Established

At the bedsideAcutely: euphoria, dissociation, transient dizziness, complete recovery. Chronically: reported psychiatric disturbance and cognitive complaints, harder to attribute given the polydrug context in which heavy use usually occurs.

Timeline of effects

Nitrous oxide — the library's longest latent phase

Time

What you seeWhat is happening

0–30 sInhalation
What you seeEuphoria, dissociation, auditory distortion, laughter.
What is happeningNMDA receptor antagonism. Onset limited by circulation time — the blood–gas partition coefficient is very low, so equilibration is almost immediate.
1–5 minOffset
What you seeComplete recovery. No hangover, no residual impairment.
What is happeningExhaled unchanged. The same low solubility that produced the rapid onset produces the rapid offset. Meanwhile the cobalt oxidation has already happened and is not reversed by exhaling the gas.
Days to weeksAccumulating inactivation
What you seeNothing. The user experiences a drug with no hangover and no visible cost, which is precisely why exposure escalates.
What is happeningEach exposure inactivates a further tranche of cobalamin.³ Methionine synthase activity falls; homocysteine and methylmalonic acid begin to rise. Serum B12 may stay entirely normal throughout.
Weeks to monthsFirst symptoms
What you seeDistal paraesthesiae and numbness, often in the feet and hands. Easily attributed to something else.
What is happeningLarge myelinated fibres fail first. Layzer's series described early sensory complaints preceding everything else.¹
Weeks to monthsMyelopathy declares itself
What you seeLhermitte's sign, gait ataxia, leg weakness, loss of balance, sphincter disturbance, impotence.¹ The patient may still be using, and may still feel fine acutely.
What is happeningDorsal-column and corticospinal demyelination. The exposure that caused this happened weeks ago and is not detectable in any sample taken today.
After stoppingRecovery — partial, slow, sometimes incomplete
What you seeImprovement over months with cessation and cobalamin replacement. Some deficits do not recover.
What is happeningNew cobalamin is not oxidised once exposure stops, and methionine synthase activity returns. Remyelination is slower and less complete than the enzyme recovery, which is why the neurological outcome lags so far behind the biochemistry.

Where this latent phase sits among the others

Nitrous oxide — damage accumulating to a threshold

The other 26 kinds of latent phase in this library

Amphetamines and MDMA — a hormone acting normally on a kidney behaving normally, while the patient supplies the water
Antipsychotics — a physical object in the stomach — extended-release quetiapine forming a pharmacobezoar
Arsenic — a tissue declaring on its own timetable rather than the poison's — the arsenic is excreted within days, but the nail that was growing while it circulated does not show its white transverse line for several weeks
Arsine and stibine — a red cell mass haemolysing faster than a kidney can cope with — the exposure is over, the haemolysis is silent until the urine changes colour, and the renal failure that follows is the cause of death
Beta-blockers — a repolarisation lesion waiting for an ectopic beat to fall inside it — sotalol prolongs the QT and then, for hours, nothing happens
Calcium-channel blockers — a tablet that has not yet dissolved
Carbon monoxide — an inflammatory process continuing after the poison itself has gone
Chlorine and ammonia — paraquat's cause at its shortest — the time an injured alveolar epithelium takes to leak
Cocaine — a package that has not yet failed — the calcium-channel blocker's cause moved outside the tablet, where wrapping integrity cannot be measured
Digoxin — distribution of the drug to its target — which that page argues is not a latent phase in the paracetamol sense at all
Ethylene glycol — paracetamol's cause with a different enzyme — glycolate accumulating behind glycolate oxidase while the patient looks merely drunk
GHB and GBL — not the poisoning but its withdrawal — a half-life under an hour means admission for any reason interrupts round-the-clock redosing
Hydrofluoric acid — an ion diffusing far enough to reach a nerve ending — and the thinner the solution, the further it travels before anybody feels it
Iron — a true remission — the corrosive injury settling while absorbed iron moves into the cells it will poison, so the patient improves on their way to the dangerous phase
Ketamine — nitrous oxide's cause on a longer clock — urothelial damage accumulating over months to years of repeated exposure
Lead — bone giving lead back — a store with a half-life of 10 to 30 years releasing its contents when pregnancy, lactation, menopause or osteoporosis resorbs it, so the blood concentration rises after the exposure has ended
Lithium — transport across cell membranes
Mercury — distribution on two clocks — tissue concentrations peaking within 24 hours everywhere except the brain, which is not reached until 2 to 3 days, and which then cannot let the poison out again
Methaemoglobin inducers — paracetamol's cause at its shortest — one to four hours manufacturing the toxic species
Methanol — paracetamol's cause again — formate accumulating behind a folate-dependent disposal step that primates perform poorly
Opioids — an antidote wearing off before the poison does — renarcotisation, the only gap in this set that treatment creates rather than reveals
Organophosphate insecticides — a fat store emptying — and, separately, a second and unexplained lesion declaring itself at a neuromuscular junction the first phase had already left
Paracetamol — time spent manufacturing a toxic metabolite
Paraquat — the body responding to an injury that is already complete
Sodium-channel blockade — a gap that cannot be shortened
Thallium — hair on its own clock rather than the poison's — sensory symptoms come first and the alopecia that makes the diagnosis obvious follows them, well after the interval in which treatment is recommended

The poison has left the body entirely, many times over, before the illness begins. Nitrous oxide's gap is not a delay between poison and effect; it is a delay between enough poison and effect.

What the mechanism predicts at the bedside

A normal serum B12 does not exclude the diagnosis. The vitamin is present and inactivated; the assay cannot see the oxidation state of the cobalt.³ This is the single commonest way the diagnosis is missed.
Homocysteine and methylmalonic acid are the tests that reflect the lesion, because they are the substrates immediately behind the two affected enzymes.³
Ask about canisters explicitly, and ask about quantity over time. Users do not describe it as drug use, and a single exposure history is uninformative — the exposure axis is cumulative.
A macrocytosis is supportive but its absence proves nothing. The neurology can arrive without any haematological abnormality.
Absent ankle jerks with extensor plantars in a young person is the pattern to recognise — combined peripheral and cord involvement is the syndrome's signature.¹
The acute presentation and the chronic presentation are different patients. Acutely: asphyxia, or cold injury to the airway from canister inhalation. Chronically: a myelopathy in someone who feels well between uses.
Nothing measurable today reflects the exposure that caused the damage. There is no level, no nomogram and no clearance to wait for.
Stopping is the treatment that most determines outcome, and it is the one that depends least on the hospital.
Check background B12 status and its causes, because a marginal starting reserve is the plausible reason two users with similar exposure differ.
Dialysis has no role and has never been assessed.⁵ The gas is long gone.

The antidote, from the poison's side

Hydroxocobalamin is one of the most mechanistically satisfying antidotes in toxicology and one of the least well specified. The gas has destroyed a cofactor; the antidote is the cofactor. There is no receptor to compete for, no enzyme to inhibit and no elimination to enhance — only a supply problem, created by chemistry, corrected by chemistry.

Hydroxocobalamin: Replaces oxidised cobalamin with cobalamin that can still be reduced and used by methionine synthase. The mechanistic fit is exact — though that is a reconstruction from the enzymology rather than a demonstrated clinical effect. Inferred What is not established is the dose, the route, the frequency or the duration in this indication — the drug's licensed use is for cyanide poisoning and for B12 deficiency of other causes, and neither regimen was designed for this.
Stopping the exposure: The intervention with the strongest claim to change outcome, and the only one that removes the cause. Continued use while receiving cobalamin re-oxidises what is given.
Methionine: Superficially the obvious replacement — supply the product of the blocked reaction. Gernez and colleagues, having found methionine within the physiological range across all four severity groups, explicitly counsel caution about its therapeutic use here.⁴ The most direct-looking intervention is the one their data least support.
Folate: Repairs the haematology and does not repair the cord, because the myelin lesion lies downstream of S-adenosylmethionine rather than in the folate cycle. This is the basis of the long-standing caution against replacing folate without cobalamin. Inferred
Naloxone, flumazenil, any receptor antagonist: No role. There is no receptor occupancy to reverse — the acute NMDA antagonism has already worn off by itself, and the chronic lesion is metabolic.
Extracorporeal removal: Never assessed and not applicable. EXTRIP has published no recommendation covering nitrous oxide.⁵

Critical appraisal

The methionine-deficiency explanation for the myelopathy carries a traditional-teaching badge on the strength of a citation for the doubt. Gernez and colleagues found plasma methionine within the physiological range (16–23 µmol/L) in all four severity groups of 93 users, and conclude that a methionine decrease cannot be imputed as the only mechanism involved, and that other pathophysiological mechanisms probably need to be identified.⁴ That contests the claim rather than merely failing to support it. The enzyme block itself is not in doubt — the same paper confirms it through the inverse methionine–homocysteine correlation.
Layzer's 1978 series is the foundational human description and is a case series of 15 people, 13 of whom were also abusing the gas and all but one of whom were dentists.¹ It establishes the syndrome; it does not establish incidence, dose–response or prognosis, and nothing on this page should be read as if it did.
Deacon's 1978 demonstration of selective B12 inactivation was in rats, and it found only ONE of the two enzymes affected.² Its abstract reports methionine synthetase rapidly inactivated and methylmalonyl-CoA mutase seemed to be unaffected. The page's two-enzyme architecture therefore rests on the 2022 review³ and on the human methylmalonic acid literature, not on Deacon — an earlier draft cited Deacon as the animal counterpart of the dual lesion, which its own abstract contradicts. The audit caught it.
The 'why these tracts' account is inference from myelin turnover, offered on the organ card as the conventional explanation and marked as contested. It is worth noticing that Layzer's own electrodiagnostic findings pointed to an axonal polyneuropathy¹, which sits awkwardly with a purely demyelinating story.
No exposure threshold appears anywhere on this page, and none should. The dose axis is cumulative and unmeasured, individual susceptibility varies with background B12 status, and any number offered would be a false precision attached to a real risk.
The vascular/thrombotic organ card is the weakest on the page and is marked as inference. Hyperhomocysteinaemia is associated with thrombosis in other settings; that association is not the same as a demonstrated causal chain in nitrous oxide users, and the case-report literature cannot supply one.
Hydroxocobalamin's regimen in this indication is not established. The mechanism argues strongly for it; the mechanism is not evidence of a dose. Anything specific belongs to TOXBASE and NPIS.
EXTRIP's silence here is genuinely uninformative rather than a gap worth noting.⁵ It is recorded for consistency with the rest of the library, not because a recommendation is awaited.

References

1
Layzer RB. Myeloneuropathy after prolonged exposure to nitrous oxide. Lancet 1978 Dec 9;2(8102):1227–30. PMID 82736. (15 patients, all but one dentists; 13 had abused the gas for 3 months to several years and 2 were exposed occupationally alone; Lhermitte's sign, gait ataxia, sphincter disturbance; electrodiagnostics indicated an axonal polyneuropathy; picture similar to that of subacute combined degeneration of the spinal cord.)
2
Deacon R, Lumb M, Perry J, et al. Selective inactivation of vitamin B12 in rats by nitrous oxide. Lancet 1978 Nov 11;2(8098):1023–4. PMID 82036. (Rats. "Exposure of rats to nitrous oxide rapidly inactivated the cytosol enzyme, methionine synthetase, but the mitochondrial enzyme, methylmalonyl CoA mutase, seemed to be unaffected, although both enzymes require vitamin B12." The selectivity in the title is between the two cobalamin enzymes — so this paper supports the methionine synthase limb and not the mutase limb.)
3
Joncquel Chevalier-Curt M, Grzych G, Tard C, et al. Nitrous oxide abuse in the emergency practice, and review of toxicity mechanisms and potential markers. Food and Chemical Toxicology 2022 Apr;162:112894. PMID 35219765. (Pathogenesis begins with oxidation by nitrous oxide of coordinated cobalamin cobalt ions; methionine synthase is inactivated and methylmalonyl-CoA mutase cofactor-depleted; reframes the disease as a pathology of DNA/RNA/protein methylation; homocysteine as the practical diagnostic marker.)
4
Gernez E, Deheul S, Tard C, et al. Plasma methionine and clinical severity in nitrous oxide consumption. Toxics 2022 Dec 23;11(1):12. PMID 36668738. (93 chronic users in four severity groups; methionine correlated with severity, Spearman −0.42, p < 10⁻⁵, and inversely with homocysteine, −0.57, p < 10⁻⁹; average methionine in all four groups within the physiological range 16–23 µmol/L; concludes a methionine decrease cannot be imputed as the only mechanism and counsels caution about therapeutic methionine.)
5
EXTRIP Workgroup — published recommendations index. Extracorporeal Treatments in Poisoning Workgroup. Cited for the absence of any recommendation covering nitrous oxide. extrip-workgroup.org/recommendations

Nitrous oxide

At a glance