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PubMed1996

Characterization of the cdhD and cdhE genes encoding subunits of the corrinoid/iron-sulfur enzyme of the CO dehydrogenase complex from Methanosarcina thermophila.

The CO dehydrogenase enzyme complex from Methanosarcina thermophila contains a corrinoid/iron-sulfur enzyme composed of two subunits (delta and gamma). The cdhD and cdhE genes, which encode the delta and gamma subunits, respectively, were cloned and sequenced. The cdhD gene is upstream of and separated by 3 bp from cdhE. Both genes are preceded by apparent ribosome-binding sites. Northern (RNA) blot and primer extension analyses indicated that cdhD and cdhE are cotranscribed from a promoter located several kilobases upstream of cdhD. The putative CdhD and CdhE sequences are 37% identical to the sequences deduced from the genes encoding the beta and alpha subunits of the corrinoid/iron-sulfur enzyme from Clostridium thermoaceticum. The CdhE sequence had a four-cysteine motif with the potential to bind a 4Fe-4S cluster previously identified in the corrinoid/iron-sulfur enzyme by electron paramagnetic resonance spectroscopy. A T7 RNA polymerase/promoter system was used to produce CdhD and CdhE independently in Escherichia coli. The purified CdhD protein was reconstituted with hydroxocobalamin in the base-on configuration. The purified CdhE protein exhibited an Fe-S center and base-off cobalamin binding in which the benzimidazole base nitrogen atom was no longer a lower axial ligand to the cobalt atom.

Aldehyde Oxidoreductases↗

PubMed1974

Some metabolic effects of sodium nitroprusside in man.

The infusion of sodium nitroprusside during surgical operations produced plasma levels of cyanide of up to four times the control value. Plasma thiocyanate showed little change except during prolonged infusion of the drug, but total plasma B(12) tended to fall, as did methylcobalamin. Other cobalamins showed little change after nitroprusside infusion for short periods. During longer infusions the ratio of methylcobalamin to adenosyl + hydroxocobalamin fell and cyanocobalamin concentrations were high.

Anesthesia, General↗

PubMed1982

Neurological involvement in hereditary transcobalamin II deficiency.

A case of hereditary transcobalamin II deficiency with neurological involvement is described. The patient presented in early infancy with megaloblastic anaemia and was treated with folinic acid from 6 weeks of age. The diagnosis of transcobalamin II deficiency was not made until he was 2 years old when he showed severely retarded intellectual development, ataxia and pyramidal deficit in the limbs. Following treatment with hydroxocobalamin, his condition has slowly improved but he has remained with a severe neurological deficit. The consequences of vitamin B12 deficiency on neurological development in infancy are discussed.

Age Factors↗

PubMed1980

West Indian amblyopia.

A series of 21 patients admitted to St Thomas' Hospital, Medical Ophthalmology Unit, with a diagnosis of West Indian or West African amblyopia is reported. Patients were investigated for haematological, biochemical, serological, and radiological abnormalities and particular attention was paid to dietary history. Patients admitted in recent years also underwent neurophysiological investigations. No definite correlation between visual loss and dietary or family history was found, and there was no evidence that the improvement in vision which occurred in just under half the patients on follow-up was related to treatment with hydroxocobalamin or multivitamins. Visual-evoked responses in 4 patients showed a prolonged latency suggesting optic nerve demyelination, while in only one case was the electro-oculogram definitely subnormal. These findings contrast with those in 'toxic' amblyopias and suggest that the syndrome of West Indian amblyopoa may be due to bilateral optic nerve demyelination of unknown aetiology rather than the effect of toxic substances or nutritional deficiency on the retina.

Adolescent↗

PubMed1998

Heme oxygenase-1 induction in skeletal muscle cells: hemin and sodium nitroprusside are regulators in vitro.

The heat shock protein heme oxygenase-1 (HO-1) is regulated by a variety of physiological and pharmacological factors. In skeletal muscle tissue, HO-1 has been shown to be induced only by exercise and electrical stimulation in vivo. Both hemin and sodium nitroprusside (SNP) are potent inducers of HO-1 in other tissues. In this study, we examined the effects of these two agents on HO-1 induction in L6.G8 rat skeletal myoblast cells. Hemin and SNP increased cellular heme oxygenase activity in both a time- and concentration-dependent manner. Increases in the HO-1 mRNA level and protein expression accompanied changes in heme oxygenase activity. The ability of SNP to induce HO-1 in L6.G8 cells was reduced by coincubation with hydroxocobalamin, a known nitric oxide (NO) scavenger, suggesting that NO itself may be involved in HO-1 gene stimulation. These results indicate that HO-1 expression is sensitive to both hemin and SNP in skeletal myoblast cells and may indicate an important regulatory mechanism of heme catabolism in skeletal muscle tissue.

Animals↗

PubMed1997

Low serum vitamin B12 levels in chronic high-flux haemodialysis patients.

The occurrence of vitamin B12 (B12) deficiency in chronic haemodialysis patients and the need for its supplementation in these patients are still matters of debate. We measured serial predialysis serum B12 levels, at 3- to 6-month intervals, in 67 unselected patients on our high-flux haemodialysis programme. Over a 12-month period, there was a significant fall in serum B12 from 497 +/- 200 (SD) to 391 +/- 131 ng/l (p < 0.001). 22 patients developed subnormal serum B12 levels and were commenced on hydroxocobalamin supplements. We were unable to demonstrate B12 clearance during dialysis using blood side studies. Measurement of B12 in the dialysate showed that 0-4.5 microg B12 was cleared per dialysis. Using these B12 measurements, in vivo B12 clearance was estimated at 9.1 ml/min. Dietary studies on 24 unselected patients showed borderline or low B12 intake in 4 patients. Absorption studies by whole-body counting on 6 patients using 57Co and 58Co showed normal B12 absorption. The same radioisotope studies demonstrated no B12 adsorption to the dialyser membrane. This study demonstrates that low serum B12 levels occur in high-flux haemodialysis patients and that losses during dialysis and dietary deficiency may be contributing factors.

Adsorption↗

PubMed2004

Nitric oxide donor sodium nitroprusside dilates rat small arteries by activation of inward rectifier potassium channels.

The role of vascular smooth muscle inward rectifier K+ (K(IR)) channels in the mechanisms underlying vasodilation is still unclear. The hypothesis that K(IR) channels are involved in sodium nitroprusside (SNP)-induced dilation of rat-tail small arteries was tested. SNP relaxed tail small arteries with an EC50 of 2.6x10(-8) mol/L. Endothelium removal did not attenuate this effect. Vessel pretreatment with hydroxocobalamin, a nitric oxide (NO) scavenger, but not with rhodanese and sodium thiosulfate, inactivators of cyanide (CN), abolished the SNP effect. Vessel pretreatment with 10(-5) mol/L Ba2+, a specific blocker of K(IR) channels at micromolar concentrations, reduced the SNP effect. Low concentrations of K+ dilated the vessels; this effect was attenuated largely after pretreatment with 3x10(-5) mol/L Ba2+. In freshly isolated smooth muscle cells, a barium-sensitive current was observed at potentials negative to the potassium equilibrium potential. Application of 10(-4) mol/L SNP increased the barium-sensitive current 1.79+/-0.23-fold at -100 mV and hyperpolarized the membrane potential by 8.6+/-0.5 mV. In tissue from freshly dissected vessels, transcripts for K(IR) 2.1 and 2.2, but not for K(IR) 2.3 and 2.4, were found. However, only K(IR) 2.1 antibodies immunostained the tunica media of the vessel. These data suggest that vascular smooth muscle K(IR) 2.1 channels are involved in the SNP-induced dilation of rat-tail small arteries.

Animals↗

PubMed2005

Life-threatening interaction between complementary medicines: cyanide toxicity following ingestion of amygdalin and vitamin C.

OBJECTIVE: To describe a case of severe accidental cyanide poisoning following a single ingestion of amygdalin with therapeutic intent. CASE SUMMARY: A 68-year-old patient with cancer presented to the emergency department shortly after her first dose (3 g) of amygdalin with a reduced Glasgow Coma Score, seizures, and severe lactic acidosis requiring intubation and ventilation. The patient also ingested 4800 mg of vitamin C per day. She responded rapidly to hydroxocobalamin treatment. The adverse drug reaction was rated probable on the Naranjo probability scale. DISCUSSION: Amygdalin and laetrile (a synthetic form of amygdalin) are commonly used as complementary or alternative medicine (CAM) for the treatment of cancer. Vitamin C is known to increase the in vitro conversion of amygdalin to cyanide and reduce body stores of cysteine, which is used to detoxify cyanide. Amygdalin has been used for decades by patients with cancer who are seeking alternative therapies, and severe reactions have not been reported with this dose. An interaction with vitamin C is a plausible explanation for this life-threatening response. CONCLUSIONS: This case highlights the fact that CAMs can produce life-threatening toxicity. This case also adds a further note of caution, namely, the potential for serious interactions between CAMs, particularly where there is no tradition of concomitant use.

Acidosis↗

PubMed2001

[Biermer's disease].

Pernicious anaemia is an autoimmune atrophic gastritis inducing vitamin B12 deficiency by malabsorption. This disease may be diagnosed in the absence of any anaemia, on a neuropathy or when one or several autoimmune disorders co-exist. Typically, pernicious anaemia is revealed by macrocytic megaloblastic anaemia. Diagnosis is done on low serum vitamin B12, raised serum homocysteine, parietal cell and, intrinsic factor antibodies. Pernicious anaemia should be treated indefinitely by monthly intramuscular hydroxocobalamin. Because of an increased incidence of gastric carcinoma, endoscopy should be evenly performed.

Anemia, Pernicious↗

PubMed2003

[Gas poisoning].

Poisoning by gases in our area is an important problem due to its high incidence. In the specific case of carbon monoxide poisoning, this is the main cause of death by poisoning in our environment, on many occasions coexisting with cyanide poisoning. Both poisonings can be severe, their diagnosis being based on the mere suspicions of the doctor. Besides, their importance lies in the fact that both poisonings have a very specific treatment. Normo or hyperbaric oxygenotherapy is the treatment for carbon monoxide poisoning. In the case of cyanide poisoning, hydroxocobalamin is nowadays the treatment of choice, since it has proved itself to be an efficient antidote.

Acute Disease↗

PubMed1992

Bitter cassava poisoning in eight children: a case report.

Bitter cassava poisoning in 8 children is reported. The incidence of bright cherry-red blood is emphasized. These patients were in bad condition, but they survived although they received different therapies. Four of them were treated with sodium nitrite and thiosulfate and the remainder with hydroxocobalamin alone. This latter drug may be useful in less severe circumstances.

Antidotes↗

PubMed1990

Studies of cobalamin as a vehicle for the renal excretion of cyanide anion.

To examine the ability of hydroxocobalamin (vitamin B12a, HO-Cbl) to counteract the toxicity of cyanide by promoting the renal excretion of cyanide anion, we studied the pharmacokinetics of HO-Cbl and cyanocobalamin (vitamin B12, CN-Cbl) given in high doses to dogs. After administration of intravenous bolus doses of HO-Cbl and CN-Cbl (5, 10, 25 mg/kg) to female foxhounds, peak plasma concentrations were attained within 1 minute, after which the cobalamins disappeared from plasma in a manner consistent with two-phase distribution and elimination kinetics. While mean t1/2 measurements for the initial distribution phase were similar for HO-Cbl and CN-Cbl, the secondary excretion phase was more prolonged for HO-Cbl than for CN-Cbl (t1/2, 94.75 minutes vs 62.64 minutes, respectively). Pharmacokinetic data permitted the design of a HO-Cbl infusion schedule that resulted in stable plasma concentrations in test animals. When NaCN was then given intravenously to animals preloaded with HO-Cbl (20 micrograms/ml plasma), conversion of HO-Cbl to CN-Cbl in vivo, was documented by both thin-layer and high-performance liquid chromatographic analysis of successive urine samples. Moreover, in dogs preloaded with HO-Cbl (20 micrograms/ml plasma), up to 10% of the cyanide administered as NaCN infusions was recovered in urine as CN-Cbl by 60 minutes, compared with less than 0.3% in dogs not treated with HO-Cbl. In addition, under these conditions of HO-Cbl loading, the minimum doses of NaCN required to produce sublethal signs of cyanide toxicity (hypotension, tachypnea, tachycardia) were found to be increased to levels that in some cases exceeded normally lethal doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

[Therapeutic attitude in cyanide poisoning (author's transl)].

According to experimental and clinical data, the present treatment of acute cyanide poisoning depends basically on: 1) Dicobaltetracemate in cases of occupational pathology to be given at the working area, to patients with giddiness or mental confusion, 2) Oxygen by assisted ventilation, associated to hydroxocobalamine and sodium thiosulfate, to be administered after admission (patients in coma or circulatory failure). Initial cardio-respiratory arrest requires immediate cardiac massage and assisted ventilation. The rapid cyanide metabolism makes useless the dialysis methods. Frequent complications as metabolic acidosis and acute pulmonary oedema respond to symptomatic treatment. If these therapeutic measures are rapidly applied in confirmed cyanide poisoning, the notion of lethal blood level should be reconsidered. Survivals have been observed with initial plasma levels of 6 mg/l.

Antidotes↗

PubMed1977

Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema.

Massive cyanide poisoning occurred in a 21-year-old man who had ingested 600 mg of potassium cyanide. The clinical course was marked by acute pulmonary edema and lactic acidosis. Because the poison was unidentified until nine hours after ingestion, the patient received only supported treatment which included diuresis, oxygen, bicarbonate, and assisted ventilation. A review of the literature shows that many case reports are poorly documented and do not provide a firm basis for evaluating therapy. To our knowledge, only four patients, including ours, have had blood levels of cyanide measured. In the absence of a suitable history, diagnosis of cyanide poisoning is difficult. A simple chemical test which can be performed on gastric aspirate is available. Hydroxocobalamin may be used as a nontoxic specific antidote. Nonspecific supportive therapy is of great importance.

Acidosis↗

PubMed1993

Subacute combined degeneration with high serum vitamin B12 level and abnormal vitamin B12 binding protein. New cause of an old syndrome.

Subacute combined degeneration of the spinal cord due to vitamin B12 deficiency invariably has been associated with a low serum vitamin B12 level. We describe a young man who presented with a unique syndrome of subacute combined degeneration associated with high serum vitamin B12 level, low red blood cell vitamin B12 level, and an abnormal plasma vitamin B12-binding protein. Uptake of cobalamin by his leukocytes in vitro was inhibited by his own but not by normal control plasma. Intensive hydroxocobalamin (vitamin B12) treatment was associated with clinical and electrophysiologic recovery accompanied by normalization of mean corpuscular volume, red blood cell vitamin B12 level, plasma homocysteine, and urinary methylmalonic acid. The subacute combined degeneration was probably precipitated by treatment with folic acid as the significance of his high serum vitamin B12 level was not apparent when he first presented with megaloblastic anemia 3 years earlier. To our knowledge, this is the first example of neurologic disease associated with high serum vitamin B12 level and provides further evidence that sometimes a serum vitamin B12 level may not be a reliable guide to vitamin B12 deficiency.

Adult↗

PubMed1977

The early phase in Leber hereditary optic atrophy.

Clinical, ophthalmoscopic, perimetric, and color vision tests and visual evoked responses were recorded in symptomatic and asymptomatic eyes in five members of a family with Leber hereditary optic atrophy. The presymptomatic eyes showed abnormalities in the retinal nerve fiber layer. Optic nerve dysfunction was found before central vision failed. The appearance of degenerating retinal nerve fibers, particularly in the papillomacular bundle, was documented photographically in the weeks after the onset of visual symptoms. Treatment with prednisone and hydroxocobalamin did not reverse or halt serious impairment of vision.

Adolescent↗

PubMed1987

Vitamin B12 responsive homocystinuria and megaloblastic anemia: heterogeneity in methylcobalamin deficiency.

A male infant with methyl-B12 deficiency (cblE) presented at age 6 weeks with lethargy, staring spells, and vomiting. He later became hypotonic and unresponsive to stimuli and required intubation and ventilation. He had homocystinuria and hypomethioninemia with megaloblastic anemia but normal serum folate and vitamin B12 concentrations. No methylmalonic aciduria was detected. Fibroblasts, cultured from the patient, were unable to grow in medium in which homocysteine replaced methionine and incorporated abnormally small amounts of [14C]-methyl-tetrahydrofolate but normal amounts of [14C]-propionate into protein. Methyl-B12 content of fibroblasts was low, while the adenosyl-B12 content was normal. Methionine synthase activity was decreased when the assay was performed under both optimal and suboptimal reducing conditions, suggesting heterogeneity in the cblE disease. The patient responded dramatically to hydroxocobalamin treatment. Homocystinuria disappeared after 10 days of therapy, and methionine was normalized after 3 weeks. Psychometric testing at age 15 months showed a developmental age of 9 months.

Anemia, Macrocytic↗

PubMed1989

Defective lysosomal release of vitamin B12 (cb1F): a hereditary cobalamin metabolic disorder associated with sudden death.

Here we report on a girl who presented with failure to thrive, developmental delay, minor facial anomalies, stomatitis, skin rashes, macrocytosis, mild homocystinemia(uria), and methylmalonic acidemia(uria). Fibroblast studies showed abnormal intracellular cobalamin (vitamin B12) metabolism. Reduced incorporation of 14C from [14C] propionate and [14C] methyltetrahydrofolate into TCA-precipitable macromolecules reflected decreased synthesis of adenosylcobalamin and methylcobalamin respectively. The diagnosis of cb1F mutation was established by demonstrating the accumulation of unmetabolized free cyanocobalamin in fibroblasts and by lack of genetic complementation with fibroblasts from the only other known cb1F patient. The defect is in the lysosomal release of endocytosed cobalamin. Administration of hydroxocobalamin resulted in clinical and biochemical improvement but sudden death occurred at age 5 months. The absence of brain pathological changes suggests that early treatment may prevent the neurological complications in cobalamin cofactor deficiency.

Female↗