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Hydroxy B12

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Hydroxy B12

$29.75 CAD

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AOR CODE: AOR04325

Helps Rid the Body of Cyanide

  • A unique form of B12 

  • Required for methylation cycles

  • Lozenges sweetened with xylitol

Use this product for: Detoxification
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Details

AOR Hydroxy B12 is hydroxocobalamin delivered in a sublingual lozenge. Cyanocobalamin, the most common form of supplemental B12, must be converted first into hydroxocobalamin, and then into adenosylcobalamin, before it can be utilized by the body. Taking hydroxocobalamin allows the body to skip a step in this conversion process, allowing for faster absorption. 

Scientists have identified B12 deficiencies as risk factors for a multitude of conditions, including neuropathy, neurodegenerative diseases, anemia, cardiovascular problems and mood imbalances, among others. B12 supplements in general are especially important for vegetarians and to help prevent pernicious anemia. Hydroxocobalamin in particular also has the unique ability to help the body to rid itself of cyanide, both by reacting with the toxin to form cyanocobalamin (which can then be excreted) and by enhancing the detoxification of cyanide through its conversion into the less toxic thiocyanate.

Hydroxy B12 provides an active and well-absorbed form of B12 for people looking to treat or prevent deficiency and anemia in an easy to consume lozenge. It has the additional benefit of helping the body eliminate toxic cyanide. 

Label Info

Discussion

Hydroxocobalamin is a storage form of B12 which can be easily converted to the active form of B12 as needed. Hydroxy B12 helps to form healthy red blood cells, and metabolize carbohydrates, fats and proteins.

Product Variation

Product Code NPN Size
AOR04325 80005478 60 LOZENGES

Supplements Facts

Serving Size: 1 Lozenge Amount % Daily
B12 (Hydroxocobalamin) 1000 mcg

xylitol, sodium stearyl fumarate, microcrystalline cellulose, rice syrup organic, hyprolose.

Guarantees

AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal byproduct.

Adult Dosage

Take 1 lozenge under the tongue daily with/without food, or as directed by a qualified health care practitioner.

Cautions

None known.

Source

Pharmaceutical synthesis

Main Application

Pernicious anemia

Superior B12 supplement

Cyanide toxicity

Disclaimer

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.

Research

Background

Hydroxocobalamin is a unique form of vitamin B12 that is especially effective for those concerned with chronic low-level cyanide toxicity. Hydroxocobalamin is more readily converted into the coenzyme forms than conventional cyanocobalamin. A coenzyme is a factor needed for the effective functioning of one of the body’s vital enzymes. Many vitamins, including B12, are not biologically active in the form in which they are normally found in food, but are instead used by the body as part of a coenzyme. In other words, in these cases, the body has to convert a vitamin into its coenzyme form in order for the vitamin to exert its biological function.

Or, in the case of vitamin B12: not function, but functions…

The Various Co-Enzyme Forms of Vitamin B12

The body uses vitamin B12 in the form of two different coenzymes, each of which plays a different role in the body. Adenosylcobalamin [also known as cobamamide or dibencozide], was discovered earlier, and is the better-known of these coenzymes. Methylcobalamin is the other coenzyme form of B12. Methylcobalamin prevents the creeping numbness, dementia, and spongy degeneration of the nerve cells (neurons) seen in B12 deficiency. Adenosylcobalamin helps the body to process some amino acids, and to form substances used in the body’s energy cycle. One coenzyme can’t substitute for the other, any more than you can use your house keys to start your car.

You might think that this is the kind of obscure little factoid that gets put into biology textbooks or turns up on Final Jeopardy, but which has no real-world importance. “My diet and supplement program includes plenty of B12,” you might think, “so my body will make all the B12 coenzymes I could ever want or need.” Like the old song says, It ain’t necessarily so.

Are You Making Enough B12?

While a good diet and supplement program usually guarantees the body a generous supply of adenosylcobalamin (unless you have a deadly genetic defect), the same cannot be said of Methylcobalamin. While adenosylcobalamin is readily stored up in the liver (and, to a lesser extent, the kidneys and other tissues), methylcobalamin’s job requires that it be free to circulate in body fluids like cytosol (the liquid medium of the cell), plasma, and the fluid that bathes the brain and spinal cord (cerebrospinal fluid). Because of this, Methylcobalamin doesn’t hang around in the body for very long.

Thus, while a person getting enough of the basic vitamin (cobalamin) will always have plenty of adenosylcobalamin, the nervous system has no special store of protective Methylcobalamin on which to rely. In fact, the body’s Methylcobalamin “fuel tanks” can easily be brought below optimal levels, and the supply is quickly depleted if it is not constantly replenished.

Skip A Step

When you take a regular B12 (cyanocobalamin) supplement, the body must first convert its B12 into hydroxocobalamin in order to form the B12 coenzymes. This involves the removal and detoxification of the cyanide molecule, followed by biochemical reduction to a less oxidized ( 1 valence) state, and then the enzymatic conversion of the reduced cobalamin into one of two metabolically active coenzyme forms. By taking a preformed hydroxocobalamin supplement, you can skip over this first biochemical stumbling block, allowing for unhampered formation of adenosylcobalamin and methylcobalamin.

Methylcobalamin or Hydroxycobalamin?

Because the body can interconvert the two B12 coenzymes, and because the body stores adenosylcobalamin but not methylcobalamin, an adequate supply of methylcobalamin usually ensures that you’ll have plenty of adenosylcobalamin, too – but not vice-versa. Because of this fact, and because of the powerful neuroprotective effects of methylcobalamin, a fully-formed methylcobalamin supplement is the best choice for most people.

Cyanide Toxicity

One key exception is persons with known or suspected cyanide toxicity, where hydroxocobalamin has an unique role to play. Hydroxocobalamin helps the body to rid itself  of cyanide, both by reacting with the toxin to form cyanocobalamin (which can then be excreted) and by enhancing the detoxification of cyanide through its conversion into the less toxic thiocyanate. In isolated human cells, hydroxocobalamin penetrates cyanide-laden cells and detoxifies the toxin directly. Hydroxocobalamin has a long history of intravenous use for acute, life-threatening cyanide toxicity (such as during industrial disasters) and is approved for this use in many European countries. At lower doses, oral hydroxocobalamin increases the urinary excretion of thiocyanate in laboratory animals fed cyanide-containing diets. Sublingual hydroxocobalamin is an ideal choice for a B12 supplement in persons concerned with chronic, low-level cyanide toxicity.

 

Research

Homocysteine Reduction for Cognitive Function

In a single-blind, placebo controlled study, it investigated the effects of a treatment of hydroxocobalamin on 16 healthy elderly subjects with low plasma Cbl concentration, but who were without cerebral and cognitive abnormalities. After one month of treatment with a placebo and then five months of treatment with intramuscular injections of hydroxocobalamin, it was determined that after supplementation with the cobalamin, plasma Cbl concentrations increased, and plasma MMA and tHcy concentrations decreased. Before and after the measurements were taken for levels of plasma cobalamin, total homocysteine (tHcy), methylmalonic acid (MMA), quantitative electroencephalograph (qEEG), and psychometric tests were taken. Improvements were observed on Verbal Word Learning Test and Verbal Fluency; electrographic signs also indicated improved cerebral function and improved cognitive function. These improvements were related to a reduction of plasma tHcy concentration.

Cyanide Exposure

Another study investigated the effects of administering hydroxocobalamin to firefighters who have suffered from hydrogen cyanide smoke inhalation, in order to determine if an early intervention with the administration of vitamin b12 coenzyme could have a positive effect. 161 firefighters who were suspected or confirmed to have hydrogen cyanide poisoning were studied in a multicenter retrospective case review from the Emergency Medical Assistance Unit (Service d’Aide Médical d’Urgence) in France. All patients were given an initial dose of 5 g of hydroxocobalamin. Non-responders received a second dose of 5 g of hydroxocobalamin. Of the patients that were initially in cardiac arrest, 30 died at the scene, 24 died in hospital, and 5 survived without cardiovascular sequelae. An improvement in cardiac disorders was noted with increasing doses of hydroxocobalamin. With higher dose administrations of the antidote, a superior outcome in patients with an initial cardiac arrest was observed.

 

Market Trends

More and more evidence continues to emerge regarding the function and importance of vitamin B12 intake. This vitamin is essential as it cannot be manufactured in the body and must be obtained through the diet. In addition, many vitamins, including B12, are not biologically active in the form in which they are normally found in food.

Methylcobalamin is the most preferable source of vitamin B12 because of its excellent bioavailability and its benefits for nerve function. Hydroxocobalamin is a lesser known coenzyme form of B12 which originates after the conversion of methylcobalamin by the body in order for it to be biologically active.

 

AOR Advantage

Hydroxocobalamin is a unique form of vitamin B12, which is more readily converted into the active coenzyme form than conventional cyanocobalamin. AOR’s HydroxyB12 delivers the essential functions of standard vitamin B12 while at the same time ridding the body of cyanide, all in a convenient and reliable lozenge.

References

Ellis FR, Nasser S. A pilot study of vitamin B12 in the treatment of tiredness. Br J Nutr. 1973 Sep; 30(2): 277-83.

Forsyth JC, Mueller PD, Becker CE, Osterloh J, Benowitz NL, Rumack BH, Hall AH. Hydroxocobalamin as a cyanide antidote: safety, efficacy and pharmacokinetics in heavily smoking normal volunteers. J Toxicol Clin Toxicol. 1993; 31(2): 277-94.

Fortin JL, Desmettre T, Manzon C, Judic-Peureux V, Peugeot-Mortier C, Giocanti JP, Hachelaf M, Grangeon M, Hostalek U, Crouzet J, Capellier G. Source: Department of Emergency and Critical Care Medicine, Jean Minjoz University Hospital, Besançon, France. Cyanide poisoning and cardiac disorders: 161 cases. J Emerg Med. 2010 May;38(4):467-76.

Mushett C, Kelley K, Boxer G, Rickards J. Antidotal Efficacy of Vitamin B12a (Hydroxo-Cobalamin) in Experimental Cyanide Poisoning. Proc Soc Exp Biol Med. 1952 Oct; 81(1): 234-7.

Sauer SW, Keim ME. Hydroxocobalamin: improved public health readiness for cyanide disasters. Ann Emerg Med. 2001 Jun; 37(6): 635-41.

Smith AD, Duckett S. Cyanide, vitamin B-12, experimental demyelination and tobacco amblyopia. Br J Exp Pathol. 1965 Dec; 46(6): 615-22.

van Asselt DZ, Pasman JW, van Lier HJ, Vingerhoets DM, Poels PJ, Kuin Y, Blom HJ, Hoefnagels WH. Cobalamin supplementation improves cognitive and cerebral function in older, cobalamin-deficient persons. J Gerontol A Biol Sci Med Sci. 2001 Dec;56(12):M775-9.

van Asselt DZ, de Groot LC, van Staveren WA, Blom HJ, Wevers RA, Biemond I, Hoefnagels WH. Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects. Am J Clin Nutr. 1998 Aug; 68(2): 328-34.

 

Abstract

Cyanide poisoning and cardiac disorders: 161 cases.

Emerg Med. 2010 May;38(4):467-76.

Fortin JL, Desmettre T, Manzon C, Judic-Peureux V, Peugeot-Mortier C, Giocanti JP, Hachelaf M, Grangeon M, Hostalek U, Crouzet J, Capellier G.

BACKGROUND: Inhalation of hydrogen cyanide from smoke in structural fires is common, but cardiovascular function in these patients is poorly documented.

OBJECTIVE: The objective was to study the cardiac complications of cyanide poisoning in patients who received early administration of a cyanide antidote, hydroxocobalamin (Cyanokit; Merck KGaA, Darmstadt, Germany [in the United States, marketed by Meridian Medical Technologies, Bristol, TN]).

METHODS: The medical records of 161 fire survivors with suspected or confirmed cyanide poisoning were reviewed in an open, multicenter, retrospective review of cases from the Emergency Medical Assistance Unit (Service d’Aide Médical d’Urgence) in France.

RESULTS: Cardiac arrest (61/161, 58 asystole, 3 ventricular fibrillation), cardiac rhythm disorders (57/161, 56 supraventricular tachycardia), repolarization disorders (12/161), and intracardiac conduction disorders (5/161) were observed. Of the total 161 patients studied, 26 displayed no cardiac disorder. All patients were given an initial dose of 5 g of hydroxocobalamin. Non-responders received a second dose of 5 g of hydroxocobalamin. Of the patients initially in cardiac arrest, 30 died at the scene, 24 died in hospital, and 5 survived without cardiovascular sequelae. Cardiac disorders improved with increasing doses of hydroxocobalamin, and higher doses of the antidote seem to be associated with a superior outcome in patients with initial cardiac arrest.

CONCLUSIONS: Cardiac complications are common in cyanide poisoning in fire survivors.

 

Hydroxycobalamin for severe acute cyanide poisoning by ingestion or inhalation.

Am J Emerg Med. 2007 Jun;25(5):551-8.

Borron SW, Baud FJ, Megarbane B, Bismuth C.

This chart review was undertaken to assess efficacy and safety of hydroxocobalamin for acute cyanide poisoning. Hospital records of the Fernand Widal and Lariboisière Hospitals were reviewed for intensive care unit admissions with cyanide poisoning for which hydroxocobalamin was used as first-line treatment from 1988 to 2003. Smoke inhalation cases were excluded. Hydroxocobalamin (5-20 g) was administered to 14 consecutive patients beginning a median 2.1 hours after cyanide ingestion or inhalation. Ten patients (71%) survived and were discharged. Of the 11 patients with blood cyanide exceeding the typically lethal threshold of 100 micromol/L, 7 survived. The most common hydroxocobalamin-attributed adverse events were chromaturia and pink skin discoloration. Severe cyanide poisoning of the nature observed in most patients in this study is frequently fatal. That 71% of patients survived after treatment with hydroxocobalamin suggests that hydroxocobalamin as first-line antidotal therapy is effective and safe in acute cyanide poisoning.

 

Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris Fire Brigade.

Clin Toxicol (Phila). 2006;44 Suppl 1:37-44.

Fortin JL, Giocanti JP, Ruttimann M, Kowalski JJ. 

INTRODUCTION: This article reports the results of a retrospective study of 8 years of experience of the Paris Fire Brigade with the prehospital use of hydroxocobalamin. 

METHODS: The head physician at the Paris Fire Brigade extracted and summarized data from standardized forms completed at the fire scene and, when available, hospital reports to assess survival status and clinical parameters associated with the use of hydroxocobalamin for each patient who received it for smoke inhalation-associated cyanide poisoning from 1995 to 2003. 

RESULTS: Of the 101 patients administered hydroxocobalamin, 30 survived, 42 died (17 at the fire scene and 25 at the intensive-care unit), and survival status was not known in the remaining 29 patients. Among the 72 patients for whom survival status was known, survival rate was 41.7% after the administration of hydroxocobalamin. Of the 38 patients found in cardiac arrest, 21 had a return of spontaneous circulation during prehospital care. Of the 12 patients who were initially hemodynamically unstable (systolic blood pressure 0 to < or =90 mmHg), 9 recovered systolic blood pressure an average of 30.6 minutes after the start of hydroxocobalamin infusion. Among nonsedated patients in the sample as a whole (n = 52), mean (SD) Glasgow coma scale score improved from 7.9 (5.4) initially to 8.5 (5.7) after administration of hydroxocobalamin. Among nonsedated patients who were initially neurologically impaired (n = 18), Glasgow coma scale score improved in 9 patients, did not change in 8 patients, and worsened in 1 patient. Two adverse events–red or pink coloration of urine or skin (n = 5) and cutaneous rash (n = 1)–were assessed as being possibly related to hydroxocobalamin. 

CONCLUSION: Hydroxocobalamin has a risk:benefit ratio rendering it suitable for prehospital use in the management of acute cyanide poisoning caused by smoke inhalation.

 

Cobalamin supplementation improves cognitive and cerebral function in older, cobalamin-deficient persons.

J Gerontol A Biol Sci Med Sci. 2001 Dec;56(12):M775-9.

van Asselt DZ, Pasman JW, van Lier HJ, Vingerhoets DM, Poels PJ, Kuin Y, Blom HJ, Hoefnagels WH.

BACKGROUND: Mild cobalamin (Cbl) deficiency is frequently found in older persons and is associated with cognitive and cerebral abnormalities. The effects of Cbl supplementation on these abnormalities are largely unknown.

METHODS: In a single-blind, placebo-controlled intervention study, 16 healthy community-dwelling elderly subjects with low plasma Cbl concentration and no cognitive impairments were studied. Subjects underwent 1 month of treatment with placebo, followed by 5 months of treatment with intramuscular injections of hydroxycobalamin. Before and after measurements of plasma cobalamin, total homocysteine (tHcy), methylmalonic acid (MMA), quantitative electroencephalograph (qEEG), and psychometric tests were taken.

RESULTS: After Cbl supplementation, plasma Cbl concentrations increased, and plasma MMA and tHcy concentrations decreased. The performance on the Verbal Word Learning Test, Verbal Fluency and Similarities improved. qEEG showed more fast activity and less slow activity. Lower plasma tHcy concentrations were related to increased fast activity on qEEG on the one hand and improved performance on the Verbal Word Learning Test and Similarities on the other. Increased fast or decreased slow activity on qEEG was associated with improved performance on the Verbal Word Learning Test, Similarities and Verbal Fluency.

CONCLUSIONS: Electrographic signs of improved cerebral function and improved cognitive function were found after Cbl supplementation in older subjects with low plasma Cbl concentrations who were free of significant cognitive impairment. These improvements were related to a reduction of plasma tHcy concentration.

 

Hydroxocobalamin: improved public health readiness for cyanide disasters.

Ann Emerg Med. 2001 Jun; 37(6): 635-41.

Sauer SW, Keim ME.

The United States is under the constant threat of a mass casualty cyanide disaster from industrial accidents, hazardous material transportation incidents, and deliberate terrorist attacks. The current readiness for cyanide disaster by the emergency medical system in the United States is abysmal. We, as a nation, are simply not prepared for a significant cyanide-related event. The standard of care for cyanide intoxication is the cyanide antidote kit, which is based on the use of nitrites to induce methemoglobinemia. This kit is both expensive and ill suited for out-of-hospital use. It also has its own inherent toxicity that prevents rapid administration. Furthermore, our hospitals frequently fail to stock this life-saving antidote or decline to stock more than one. Hydroxocobalamin is well recognized as an efficacious, safe, and easily administered cyanide antidote. Because of its extremely low adverse effect profile, it is ideal for out-of-hospital use in suspected cyanide intoxication. To effectively prepare for a cyanide disaster, the United States must investigate, adopt, manufacture, and stockpile hydroxocobalamin to prevent needless morbidity and mortality.

 

Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects.

Am J Clin Nutr. 1998 Aug; 68(2): 328-34.

van Asselt DZ, de Groot LC, van Staveren WA, Blom HJ, Wevers RA, Biemond I, Hoefnagels WH.

BACKGROUND: The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood.

OBJECTIVE: We aimed to determine the reason for this high prevalence. 

DESIGN: We examined cobalamin intake, the presence and severity of atrophic gastritis, the presence of Helicobacter pylori infection, and plasma cobalamin and methylmalonic acid (MMA) concentrations in 105 healthy, free-living, older subjects aged 74-80 y.

RESULTS: Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 micromol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin > or = 260 pmol/L and plasma MMA < or = 0.32 micromol/L). Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 microg/d. Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 microg/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 microg/d; 25th and 75th percentiles: 5.4, 7.9) (P = 0.0336), mainly because of less frequent use of cobalamin supplements (8% compared with 29.6%; chi2 = 3.9, P = 0.048). Atrophic gastritis was found in 32.4% of the total study group: mild to moderate in 19.6% and severe in 12.7%. The prevalence of severe atrophic gastritis, but not mild-to-moderate atrophic gastritis, was higher in mildly cobalamin-deficient subjects (25%) than in non-cobalamin-deficient subjects (3.7%) (chi2 = 4.6, P = 0.032). The prevalence of immunoglobulin G antibodies to H. pylori was similar in mildly cobalamin-deficient subjects (54.2%) and in non-cobalamin-deficient subjects (44.4%) (chi2 = 0.5, P = 0.5). 

CONCLUSIONS: The high prevalence of mild cobalamin deficiency in healthy, free-living, older Dutch subjects could be explained by inadequate cobalamin intake or severe atrophic gastritis in only 28% of the study population. Other mechanisms explaining mild cobalamin deficiency in older people must be sought.

 

Hydroxocobalamin as a cyanide antidote: safety, efficacy and pharmacokinetics in heavily smoking normal volunteers.

J Toxicol Clin Toxicol. 1993; 31(2): 277-94.

Forsyth JC, Mueller PD, Becker CE, Osterloh J, Benowitz NL, Rumack BH, Hall AH.

The safety, efficacy and pharmacokinetic parameters of 5 g of hydroxocobalamin given intravenously, alone or in combination with 12.5 g of sodium thiosulfate, were evaluated in healthy adult men who were heavy smokers. Sodium thiosulfate caused nausea, vomiting, and localized burning, muscle cramping, or twitching at the infusion site. Hydroxocobalamin was associated with a transient reddish discoloration of the skin, mucous membranes, and urine, and when administered alone produced mean elevations of 13.6% in systolic and 25.9% in diastolic blood pressure, with a concomitant 16.3% decrease in heart rate. No other clinically significant adverse effects were noted. Hydroxocobalamin alone decreased whole blood cyanide levels by 59% and increased urinary cyanide excretion. Pharmacokinetic parameters of hydroxocobalamin were best defined in the group who received both antidotes: t1/2 (alpha), 0.52 h; t1/2 (beta), 2.83 h; Vd (beta), 0.24 L/kg; and mean peak serum concentration 753 mcg/mL (560 mumol/L) at 0-50 minutes after completion of infusion. Hydroxocobalamin is safe when administered in a 5 gram intravenous dose, and effectively decreases the low whole blood cyanide levels found in heavy smokers.

 

A pilot study of vitamin B12 in the treatment of tiredness.

Br J Nutr. 1973 Sep; 30(2): 277-83.

Ellis FR, Nasser S.

Twenty-eight subjects complaining of tiredness completed a double-blinded cross-over trial of injections of hydroxocobalamin followed by a rest period of 2 weeks and then a similar course of matching placebo injections. Symptoms were assessed by a daily self-rating method and included appetite, mood, energy, sleep, and general feeling of well-being. Those subjects who received the placebo in the first 2-week period showed a favourable response to hydroxocobalamin in the second period in all measurements made. The response achieved statistical significance (P = 0.006) in respect of general well-being; ‘happiness’ achieved a value of P = 0.032. Subjects who received hydroxocobalamin in the first period showed no difference between responses to active and placebo treatments, which suggests that the effects of the vitamin may persist for a period of at least 4 weeks.

 

Cyanide, vitamin B-12, experimental demyelination and tobacco amblyopia.

Br J Exp Pathol. 1965 Dec; 46(6): 615-22.

Smith AD, Duckett S.

Experimental evidence is presented which shows that rats can be protected from the deleterious effects of cyanide poisoning on the central nervous system by the concomitant administration of hydroxocobalamin as opposed to commercial cyanocobalamin. It is suggested that this may be more that just a chemical binding of cyanide by the hydroxocobalamin and could have implications with respect for the integrity of myelin in general. In addition, a case of tobacco amblyopia is described and an analogy drawn between this and the experimental evidence.

 

Antidotal Efficacy of Vitamin B12a (Hydroxo-Cobalamin) in Experimental Cyanide Poisoning.

Proc Soc Exp Biol Med. 1952 Oct; 81(1): 234-7.

Mushett C, Kelley K, Boxer G, Rickards J.

Vit. B12a (hydroxo-cobalamin), but not vitamin B12 (cyano-cobalamin), has been found to be capable of preventing in mice the toxic symptoms and death due to cyanide administration. When injected into mice exhibiting complete respiratory arrest and coma due to cyanide poisoning, vit. B12a effected rapid recovery of most animals. In mice injected with potassium cyanide followed by vit. B12a, some of the cyanide appears in the urine as thiocyanate, but a greater percentage of the cyanide appears as vit. B12, having formed this compound by reacting with the vit. B12a.

 

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