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At least 73 records · Page 4Linked to original sources
PubMed1989

Thiosulphate and hydroxocobalamin prophylaxis in progressive cyanide poisoning in guinea-pigs.

The duration of action of the cyanide antidotes sodium thiosulphate and hydroxocobalamin was investigated in guinea-pigs after prophylactic administration before a long-term infusion of NaCN. The parameter for the diminution of the antidote action was the point of time at which the concentration of HCN in the exhaled air of the animals exceeded 100 nmol/kg per min. The time taken to reach this threshold level in the control animals was 12 min. While the threshold level could be extended only to 35 min with hydroxocobalamin (300 mg/kg i.v.) the protective action of sodium thiosulphate (100, 500 and 1000 mg/kg i.v.) persisted dose dependently for about 1, 2 and 4 h, respectively. Additionally we found a plasma half-life of sodium thiosulphate in guinea-pigs of 26 min. This value corresponds approximately to the plasma half-life of sodium thiosulphate in humans given in the literature. Because of the large injection volume necessary, sodium thiosulphate is not suitable for prophylactic use in man.

Animals↗
PubMed1999

Progressive neurological deterioration and MRI changes in cblC methylmalonic acidaemia treated with hydroxocobalamin.

Cobalamin C (cblC) defects result in decreased activity of both methylmalonyl-CoA mutase and N5-methyltetrahydrofolate:homocysteine methyltransferase (methionine synthase), with subsequent methylmalonic acid-uria and homocystinuria. Patients typically show failure to thrive, developmental delay and megaloblastic anaemia. Vitamin B12 therapy has been beneficial in some cases. We report a now 4-year-old Hispanic girl with cblC disease documented by complementation analysis, with progressive neurological deterioration and worsening head MRI changes while on intramuscular hydroxocobalamin begun at age 3 weeks. Oral carnitine and folic acid were added at age 1 year. Blood levels of methylmalonic acid were reduced to treatment ranges. In the absence of acute metabolic crises, she developed microcephaly, progressive hypotonia and decreased interactiveness. Funduscopic examination was normal at age 13 months. At age 19 months, she developed nystagmus, and darkly pigmented fundi and sclerotic retinal vessels were observed on examination. Her neonatal head MRI was normal. By age 1 year, the MRI showed diffuse white-matter loss with secondary third and lateral ventricle enlargement, a thin corpus callosum, and normal basal ganglia. At age 15 months, progression of the white-matter loss, as well as hyperintense globi pallidi, were present. Interval progression of both grey- and white-matter loss was seen at age 27 months. We therefore caution that progressive neurological deterioration and head MRI abnormalities may still occur in cblC disease, despite early initiation of hydroxocobalamin therapy and improvement in toxic metabolite concentrations in physiological fluids.

Brain↗
PubMed2001

Hydroxocobalamin: improved public health readiness for cyanide disasters.

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.

Accidents, Occupational↗
PubMed1976

Nitroprusside-induced cyanide poisoning: antidotal effect of hydroxocobalamin.

Sodium nitroprusside was investigated as a potential source of cyanide poisoning, Whole-blood cyanide determinations were performed on arterial samples from baboons receiving nitroprusside while anesthetized. There was a statistically significant increase in cyanide levels, as well as development of tachyphylaxis and severe metabolic acidosis. Hydroxocobalamin (vitamin B12a) infused simultaneously with nitroprusside significantly lessened the increase in cyanide levels and eliminated the development of metabolic acidosis. Nitroprusside can cause cyanide intoxication in the baboon, and hydroxocobalamin appears to be an effective antidote.

Acid-Base Equilibrium↗
PubMed1987

Hydroxocobalamin for initial and long-term therapy for vitamin B12 deficiency.

Seventeen patients were treated for vitamin B12 deficiency with i.m. injection of 1 mg hydroxocobalamin every three months as maintenance therapy for eight to 20 years after an initial depot treatment of one or two series of five i.m. injections on alternate days. In three of four patients given two depot series less than or equal to 3 months apart, and with no antibody to transcobalamin II (TC II) detected previously, abnormally high values of serum cobalamins were measured at the end of injection intervals after seven to 12 years. No increase in unsaturated B12 binding capacity (UB12BC) was found in contrast to findings in patients given identical therapy, in whom an early increase above the normal level occurred associated with antibody to TC II. One depot series followed by i.m. injection of 1 mg hydroxocobalamin every third month secured values within the normal range for serum cobalamin, UB12BC and total B12 binding capacity (TB12BC).

Delayed-Action Preparations↗
PubMed1996

Comparison of the effects of hydroxocobalamin and oxyhaemoglobin on responses to NO, EDRF and the nitrergic transmitter.

1. The effects of ranges of concentrations of oxyhaemoglobin (0.01-30 microM) and hydroxocobalamin (1-100 microM) were compared for their abilities to reduce relaxant responses to EDRF released by acetylcholine in endothelium-intact rat aortic rings, the nitergic transmitter in rat anococcygeus muscles, and NO in aqueous solution in both tissues (aortic rings were denuded of endothelium). 2. The concentrations of oxyhaemoglobin producing 50% reduction of responses to EDRF and NO in rat aorta correspond closely, the IC50 values being 0.13 +/- 0.02 microM and 0.11 +/- 0.02 microM respectively. 3. Oxyhaemoglobin was equally effective in inhibiting responses to NO in anococcygeus muscles and in aortic rings with an IC50 of 0.14 +/- 0.05 microM. However, responses to the nitrergic transmitter were considerably less sensitive to inhibition by oxyhaemoglobin, the IC50 being 19.7 +/- 5.1 microM. 4. The IC50 values for hydroxocobalamin in inhibiting responses to EDRF and NO in aorta were 3.4 +/- 0.2 microM and 8.4 +/- 0.63 microM, respectively, but it was less effective against responses to NO in anococcygeus muscles the IC50 being 46 +/- 9.6 microM. However, even in the highest concentration used (100 microM), it did not reduce responses to the nitrergic transmitter. 5. The findings are compatible with the views that EDRF is NO, but suggest that the nitergic transmitter in the rat anococcygeus muscle does not behave like free NO.

Acetylcholine↗
PubMed1976

Uptake of hydroxocobalamin by rat liver mitochondria. Binding to a mitochondrial protein.

Lysosome-free preparations of rat liver mitochondria take up hydroxo[57Co]cobalamin by a process which is dependent on mitochondrial swelling, rather than on energy or ion fluxes. The uptake system is saturable and unidirectional, leading to inside/outside concentration ratios of 17. The process also exhibits specificity: cyano[57Co]cobalamin is taken up less rapidly and to a lesser extent than hydroxocobalamin; methylcobalamin and adenoslcobalamin inhibit hydroxocobalamin uptake markedly, while cyanocobalamin does not. The [57Co]cobalamin ([57Co]Cbl) taken up is bound to a mitochondrial protein whose apparent molecular weight is 120,000 by Sephadex G-150 chromatography. Double reciprocal plots of bound [57Co]Cbl versus medium [57Co]Cbl concentration yield estimates for bound Cblmax of 29 pmol/mg of protein and for Kd is 8.2 muM. We conclude that mitochondrial uptake of cobalamins occurs via the diffusion of free cobalamins into the mitochondria and their subsequent binding to a high affinity mitochondrial protein(s) which we propose to be the source of the unidirectional character, the saturability, and the specificity of the uptake system.

Acid Phosphatase↗
PubMed1992

Multicomponent spectrophotometric assay of cyanocobalamin, hydroxocobalamin and riboflavin.

The photolysis of cyanacobalamin to hydroxocobalamin in aqueous solution is influenced by riboflavin. A multicomponent spcctrophotometric method has been developed for the simultaneous determination of cyanocobalamin, hydroxocobalamin and riboflavin in degraded solutions by absorbance measurements at 550, 525 and 445 nm. The relative standard deviation of the method is 2,5% and the recoveries range from 97.3-103.3%. The method has been applied to study the photolysis of cyanocobalamin in presence of riboflavin.

Journal Article↗
PubMed1980

The antidote effect of thiosulphate and hydroxocobalamin in formation of nitroprusside intoxication of rabbits.

Sodium nitroprusside (SNP) and hydroxocobalamin (HC) - in molar ratios of 1:4, 1:5, and 1:8, respectively - were infused simultaneously during 4 h into two veins of separate ears of conscious rabbits. Controls received HC only. Sodium thiosulphate (ST) was infused with SNP at molar ratios of 1:4, 1:5, and 1:10. The observation period was 48 h. With the lowest dose of HC (1:4), SNP produced a severe metabolic acidosis; three of ten animals died during the infusion, an additional six within 24 h. When the 1:5 ratio was administered, the acidosis was less marked, but still three of seven animals succumbed within 24 h. The highest dose (1:8) prevented acidosis, however three of eight animals died. All doses of HC caused histological changes in the liver, the myocardium, and the kidney, independently if given alone or with SNP. In contrast to this, ST had a complete antidote effect, if administered in a 1:5 ratio; no acidosis was demonstrable and death did not occur. In neither dosage ST could prevent histological changes in the liver, but the kidney and the heart were not affected. In contrast to HC ST alone did not cause histological alterations. Consequently, ST is the preferable antidote and is superior to HC for preventing or treating intoxications with SNP.

Animals↗
PubMed1980

Granulocyte dysfunction in transcobalamin II deficiency responding to leucovorin or hydroxocobalamin-plasma transfusion.

Granulocytes from a 6-year-old boy with congenital transcobalamin II (TC II) deficiency were found to have abnormally low antibacterial activity against Staphylococcus aureus and very low intracellular levels of the cobalamin coenzymes. Transfusion of hydroxocobalamin (OH-Cbl) bound to normal plasma temporarily restored granulocyte bactericidal activity and increased cellular levels of the cobalamin coenzymes. Granulocyte function was also temporarily restored by oral Leucovorin. The defect appeared to be causally related to the patient's TC II deficiency and indirectly to a deficiency of cobalamin and folate coenzymes.

Blood Proteins↗
PubMed2007

Potential interference by hydroxocobalamin on cooximetry hemoglobin measurements during cyanide and smoke inhalation treatments.

STUDY OBJECTIVE: Concentrated aqueous solutions of hydroxocobalamin (OHCob) are administered intravenously for cyanide poisoning victims, many of whom also have concurrent smoke inhalation. Because of its intense light absorbance in visible wavelengths (absorption peak at 532 nm), we investigate potential interference effects of OHCob on total hemoglobin concentration (tHb), carboxyhemoglobin (COHb), methemoglobin (MetHb), and oxyhemoglobin (Hb-O2) cooximetry measurement values in blood. METHODS: In vivo cooximetry measurements were conducted with 3 specific pathogen-free white New Zealand rabbits (3.80+/-0.21 kg) during the intravenous infusion of OHCob (625 mg during a 100-minute period). Resultant changes in tHb, Hb-O2, COHb, and MetHb values were measured and correlated with respect to estimated in vivo OHCob concentrations. In vitro measurements were conducted with rabbit blood to confirm in vivo measurements. RESULTS: The introduction of OHCob clearly interfered with the cooximetry measurements of each of the hemoglobin component fractions in whole blood and resulted in altered measurement values from the baseline values. The presence of OHCob in blood interferes with cooximetry measurements of COHb, MetHb, and Hb-O2. The increase in measured COHb fraction with increasing concentrations of OHCob was most notable. CONCLUSION: The presence of OHCob in blood interferes with cooximetry measurements of COHb, MetHb, and Hb-O2. These effects need to be considered during OHCob treatment of cyanide poisoning, particularly in smoke inhalation victims with potential for concurrent carbon monoxide exposure, because it may lead to potentially erroneous reported COHb levels.

Animals↗
PubMed2005

Electronic structure and bonding in hydroxocobalamin.

The electronic structure of hydroxocobalamin (OHCbl) has been calculated by a density functional method, using the orthogonalized linear combination of the atomic orbitals method (OLCAO). The X-ray crystal structure has been determined from synchrotron X-ray diffraction data and the geometry determined was used in the calculations. Comparison with the recently reported electronic structures of cyanocobalamin (CNCbl), methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl) shows that Mulliken charges (Q*) and bond orders (BO) vary only on the axial fragment.

Cobamides↗
PubMed2000

Picomolar quantitation of free sulfite in foods by means of [57Co]hydroxocobalamin and radiometric chromatography of [57Co]sulfitocobalamin. Method, applications and significance of coexisting sulfides.

The concentration dependent reaction of sulfite with 57Co-labeled hydroxocobalamin (OH57CoCbl) to produce a sulfitocobalamin (SO(3)57CoCbl) adduct served as a quantification strategy for foodborne sulfite residues freely extracted into pH 5.2, 0.05 M acetate buffer. SO(3)57CoCbl was then resolved using SP-Sephadex C-25 gel chromatography and its radiometric detection allowed calculation of a standard logit plot from which unknown sulfite concentrations could be determined. The sulfite detection range was 6.0 nM-0.3 pM with respective relative standard deviations of 4.4-29.4% for 50-microl samples. Individual incidences of foodborne sulfite intolerances provoked by L-cysteine or sulfite additive use in bakery products, which remained undetected using conventional sulfite analytical methods, underscored the quantitative value of the method. The analytical significance and occurrences of detectable sulfides coexisting with foodborne sulfite residues was also addressed.

Chromatography, Gel↗
PubMed1994

Effect of the cyanide antidote hydroxocobalamin on commonly ordered serum chemistry studies.

STUDY HYPOTHESIS: Concentrated aqueous solutions of hydroxocobalamin (OHCob) are given intravenously for the treatment of cyanide poisoning. Because OHCob solutions are intensely red and have peak light absorptions at 352 nm and 525 nm, we investigated whether the presence of OHCob in serum would interfere with various automated, colorimetric chemistry measurements. DESIGN: Selected serum chemistry colorimetric measurements were compared in seven patients, using their own serum as control, with serum containing OHCob at the following concentrations: 100 mg/L, 500 mg/L, and 1,000 mg/L. These concentrations are in the range achieved with therapeutic doses of OHCob when given for cyanide poisoning. MEASUREMENTS AND MAIN RESULTS: Statistically significant alterations in serum values for aspartate aminotransferase, total bilirubin, creatinine, magnesium, and iron were seen in the presence of OHCob. CONCLUSION: The presence of OHCob in serum interferes with several chemistry methodologies, and such interference should be anticipated when this antidote is used.

Adult↗
PubMed1990

[Potassium cyanide poisoning treated with hydroxocobalamin].

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.

Acidosis↗
PubMed1976

Hydroxocobalamin therapy of cyanide intoxication in guinea pigs.

The efficacy of hydroxocobalamin (vitamin B12a) as a specific, nontoxic antidote in acute cyanide poisoning was tested. Guinea pigs receiving lethal intravenous NaCN injections were treated with either vitamin B12a or saline solution. There was a statistically significant antidotal effect of the vitamin. No toxic effect was observed with large doses of the vitamin.

Animals↗
PubMed1987

31P nuclear magnetic resonance in vivo spectroscopy of the metabolic changes induced in the awake rat brain during KCN intoxication and its reversal by hydroxocobalamine.

Radiofrequency surface coils were chronically implanted in rats, which were subsequently subjected to 31P nuclear magnetic resonance (NMR) investigations at 4.7 T. The implanted coil allowed study of the animals without need for anesthesia, which is a prerequisite for studies of normal brain metabolism. The animals may be kept in the NMR probe for several hours. During subsequent experiments, they may be placed in the same position, therefore allowing follow-up studies for periods as long as 2 months. This method has been used in the study of sublethal KCN intoxication. KCN, a cytochrome c oxidase inhibitor, induces a blockade of cell respiratory processes, which is reflected, in a dose-dependent manner, by a decrease in phosphocreatine content and pH and an increase in inorganic phosphate content, whereas ATP levels remain constant until high doses of KCN (6 mg/kg i.p.) are reached. 31P NMR allows the time course of these metabolic changes to be followed. For high KCN doses, a new peak, termed X, is observed, which is interpreted as being due to a pool of inorganic phosphate at very low pH (5.65), corresponding to a subset of cells that did not survive KCN injury. Hydroxocobalamine, a specific antidote of KCN, suppresses the metabolic changes due to 6 mg/kg of KCN.

Animals↗