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PubMed2003

p38 Mitogen-activated protein kinase regulates Bax translocation in cyanide-induced apoptosis.

Execution of cyanide-induced apoptosis is mediated by release of cytochrome c from mitochondria. To determine how cyanide initiates cytochrome c release, Bax translocation was investigated in primary cultures of cortical neurons. Under nonapoptotic (control) conditions, Bax resided predominantly in the cytoplasm. After 300-microM cyanide treatment for 1 h, Bax translocated to the mitochondria, as shown by immunocytochemical staining and subcellular fractionation; Western blot analysis confirmed "cytosol-to-mitochondria" translocation of Bax. Temporal analysis showed that Bax translocation preceded cytochrome c release from the mitochondria, which was initiated 3 h after cyanide treatment. In double-immunofluorescence labeling for both Bax and cytochrome c, it was observed that cytochrome c was released only in cells showing Bax in mitochondria. The role of p38 mitogen-activated protein (MAP) kinase in Bax translocation was studied. The p38 MAP kinase was activated 30 min after cyanide, and its phosphorylation level of activity began to decrease 3 h later. SB203580, a p38 MAP kinase inhibitor, blocked translocation of Bax to mitochondria, whereas SB202474, a control peptide, had no effect on translocation. Inhibition of p38 MAP kinase by SB203580 blocked all downstream effects of Bax translocation, including cytochrome c release, caspase activation, and internucleosomal DNA fragmentation. These results demonstrated that Bax translocation is critical for cyanide-induced cytochrome c release and that p38 MAP kinase regulates Bax translocation from cytosol to mitochondria.

Animals↗
PubMed1993

Use of vitamin B12 in the treatment and prevention of nitroprusside-induced cyanide toxicity.

OBJECTIVE: To review the mechanism of action, safety, and efficacy of hydroxocobalamin in the treatment and prevention of nitroprusside-induced cyanide toxicity. DATA SOURCES: English and foreign-language journal articles and reference texts identified from Index Medicus. Both animal and human studies were included. DATA SYNTHESIS: High-dose or prolonged therapy with nitroprusside in patients with hepatic or renal dysfunction increases the risk for nitroprusside-induced cyanide or thiocyanate toxicity, respectively. Hydroxocobalamin has been shown to significantly reduce RBC and plasma cyanide concentrations in animals and surgical patients without producing clinically important adverse effects or toxic metabolites. Thiosulfate infusions also decrease cyanide toxicity but can cause accumulation of thiocyanate resulting in clinical toxicity. Cyanocobalamin cannot effectively remove cyanide due to poor binding. CONCLUSIONS: Hydroxocobalamin is a safe and effective agent in the prevention and treatment of nitroprusside-induced cyanide toxicity. Prolonged or high-dose infusions of nitroprusside should be minimized in critically ill patients, especially if hepatic and/or renal dysfunction is present.

Animals↗
PubMed1989

Cyanide release from sodium nitroprusside during coronary bypass in hypothermia.

Erythrocyte cyanide levels were determined by a sensitive fluorimetric method on four occasions during coronary bypass in hypothermia in 18 consecutive patients treated with sodium nitroprusside (SNP) with an infusion rate less than 1 microgram x kg-1 x min-1. Every second patient received the cyanide antidote thiosulphate simultaneously with the SNP-infusion. At normal body temperature, as well as during hypothermia in cases receiving thiosulphate, the cyanide levels rose slowly but significantly with the infusion rate. Higher erythrocyte cyanide levels in relation to the infusion rates, up to 8.0 mumol/l, were found during hypothermia in two of the cases not receiving thiosulphate. We conclude that SNP is broken down to cyanide even under hypothermia and that low body temperature may impair the conversion of cyanide to thiocyanate, probably by affecting the metabolic pathways providing the sulphur substrate. This effect may add to other factors decreasing sulphur availability in critically ill patients, and simultaneous administration of thiosulphate is therefore recommended to ensure a safe SNP treatment during and after coronary bypass operations.

Adult↗
PubMed1976

Regulation of cyanide-insensitive respiration in Neurospora.

1. Inhibition of either mitochondrial transcription or translation in Neurospora crassa results in the rapid production of the cyanide-insensitive pathway of mitochondrial respiration. Protein synthesis on cytoplasmic ribosomes is required for the appearance of cyanide-insensitive respiration in the culture. 2. Removal of the inhibition of transcription of translation results in a rapid return to cyanide-sensitive respiration. Additional protein synthesis in the cytoplasm is required for the loss of cyanide-insensitive respiratory activity while additional mitochondrial protein synthesis has no effect. 3. These studies indicate that a mitochondrial gene product is involved in a negative manner in the regulation of cyanide-insensitive respiration. When the mitochondrial product is present, the pathway is not expressed, when the mitochondrial product is absent, the pathway is expressed. 4. Studies with forced heterokaryons formed from respiratory-deficient mutants having cyanide-insensitive respiration and respiratory-competent auxotrophs indicate that the site of action of the mitochondrial gene product is external to the mitochondrion.

Chloramphenicol↗
PubMed1995

Expression of the cyanide hydratase enzyme from Fusarium lateritium in Escherichia coli and identification of an essential cysteine residue.

The filamentous fungus Fusarium lateritium is cyanide tolerant, due partly to the induction of the enzyme cyanide hydratase in the presence of cyanide. This enzyme catalyses the hydration of cyanide to formamide. The expression in Escherichia coli of a cDNA clone encoding cyanide hydratase is described. The cDNA cloned was expressed as a transcriptional fusion in the expression vector pKK233-2 and a high level of activity of cyanide hydratase was detected in E. coli. Site-directed mutagenesis of the cys-163 residue inactivated the enzyme.

Amino Acid Sequence↗
PubMed1980

The effects of sodium nitroprusside and cyanide on haemoglobin function.

Incubation of human blood with 0.3 mM sodium nitroprusside (SNP) or 1 mM potassium cyanide (KCN) for 180 min produced a 600-fold increase in red cell cyanide concentration, a 4% decrease in oxygen capacity and a 6% increase in oxygen affinity. These effects were not reproduced in patients receiving SNP by infusion probably because in the clinical situation much smaller amounts of the drug were used and red cell cyanide levels were lower. The in vitro observations could be explained by cyanide either combining directly with the haemoglobin or encouraging its spontaneous oxidation to methaemoglobin during the incubation. Differences in distribution of cyanide between red cell and plasma following incubation with SNP or KCN and the initial lag phase in accumulation of cyanide in the red cell with SNP provide further evidence that nitroprusside breaks down principally within the red cell.

Cyanides↗
PubMed2003

CynD, the cyanide dihydratase from Bacillus pumilus: gene cloning and structural studies.

The cyanide dihydratase in Bacillus pumilus was shown to be an 18-subunit spiral structure by three-dimensional reconstruction of electron micrographs of negatively stained material at its optimum pH, 8.0. At pH 5.4, the subunits rearrange to form an extended left-handed helix. Gel electrophoresis of glutaraldehyde cross-linked enzyme suggests that the fundamental component of the spiral is a dimer of the 37-kDa subunit. The gene was cloned, and the recombinant enzyme was readily expressed at high levels in Escherichia coli. Purification of the recombinant enzyme was facilitated by the addition of a C-terminal six-histidine affinity purification tag. The tagged recombinant enzyme has K(m) and V(max) values similar to those published for the native enzyme. This is the first cyanide dihydratase from a gram-positive bacterium to be sequenced, and it is the first description of the structure of any member of this enzyme class. The putative amino acid sequence shares over 80% identity to the only other sequenced cyanide dihydratase, that of the gram-negative Pseudomonas stutzeri strain AK61, and is similar to a number of other bacterial and fungal nitrilases. This sequence similarity suggests that the novel short spiral structure may be typical of these enzymes. In addition, an active cyanide dihydratase from a non-cyanide-degrading isolate of B. pumilus (strain 8A3) was cloned and expressed. This suggests that cynD, the gene coding for the cyanide dihydratase, is not unique to the C1 strain of B. pumilus and is not a reflection of its origin at a mining waste site.

Amino Acid Sequence↗
PubMed1971

Cyanide-resistant respiration in Neurospora crassa.

Cell respiration in wild type and poky was studied as part of a long-term investigation of cyanide-resistant respiration in Neurospora. Respiration in wild type proceeds via a cytochrome chain which is similar to that of higher organisms; it is sensitive to antimycin A or cyanide. Poky, on the other hand, respires by means of two alternative oxidase systems. One of these is analogous to the wild-type cytochrome chain in that it can be inhibited by antimycin A or cyanide; this system accounts for as much as 15% of the respiration of poky f(-) and 34% of the respiration of poky f(+). The second oxidase system is unaffected by antimycin A or cyanide at concentrations which inhibit the cytochrome chain maximally. It can, however, be specifically inhibited by salicyl hydroxamic acid. The cyanide-resistant oxidase is not exclusive to poky, but is also present in small quantities in wild type grown under ordinary circumstances. These quantities may be greatly increased (as much as 20-fold) by growing wild type in the presence of antimycin A, cyanide, or chloramphenicol.

Aerobiosis↗
PubMed1989

Leber's hereditary optic atrophy: further evidence for a defect of cyanide metabolism?

We studied one patient with Leber's optic atrophy (LOA) in the acute stage and 12 at the chronic stage of the disease, and measured the activity of rhodanese in white blood cells and the level of cyanide in whole blood. In the patient with acute disease the blood cyanide level was significantly increased at first. Treatment of this patient with cyanide antagonists reduced his cyanide level, but this was not accompanied by improvement in visual function. Rhodanese activity was normal in all patients, as were the blood cyanide levels in each of the 12 patients at the chronic stage of the disease. These findings suggest a temporary disturbance of cyanide metabolism during the acute phase of the disease in this family. The abnormal metabolic mechanism was not identified.

Acute Disease↗
PubMed1984

Whole blood cyanide levels in patients with tobacco amblyopia.

Three patients presented with painless bilateral visual failure due to tobacco amblyopia. The whole blood cyanide levels were raised above those predicted from their high tobacco consumption, approaching lethal levels reported from acute inhalation of cyanide. Each patient had an excessive alcohol intake with biochemical evidence of hepatic dysfunction, the elevated whole blood cyanide levels being attributed to the associated impairment of cyanide detoxification. In each case the improvement in visual acuities following abstinence and hydroxycobalamin therapy was accompanied by a reduction in the whole blood cyanide level to within the normal range. Serial measurements of whole blood cyanide, serum alcohol, and the detection of urinary nicotine provided valuable indices of the patient's subsequent compliance and clinical progress.

Adult↗
PubMed2003

Incidence of endemic ataxic polyneuropathy and its relation to exposure to cyanide in a Nigerian community.

BACKGROUND: The occurrence of ataxic polyneuropathy in an endemic area in south west Nigeria has been attributed to exposure to cyanide from cassava foods. However, it has been shown that the prevalence of ataxic polyneuropathy is not high in several communities in the tropics where exposure to cyanide from cassava foods is high. OBJECTIVES: To determine the incidence of ataxic polyneuropathy in an endemic community, and to compare the intake of cassava foods, exposure to cyanide, and levels of thiols in cases and controls. METHODS: A cohort of 3167 healthy subjects aged 10 years and over in Ososa, Nigeria, was followed for two years, screened, and examined neurologically. Ataxic polyneuropathy was diagnosed if sensory polyneuropathy and sensory gait ataxia were both present. Controls were selected randomly within 10 year age groups of subjects who screened negative. Intake of cassava foods, exposure to cyanide, concentrations of thiols (glutathione, cysteine, and gamma glutamylcysteine) in plasma, and visual evoked potentials were measured. RESULTS: Person-years of follow up were 6246 for 1469 male and 1698 female subjects in the cohort. The incidence of ataxic polyneuropathy was 64 per 10,000 person-years (31 for male and 93 for female subjects). Multivariate odd ratios were 0.78 (95% CI 0.23 to 2.61) for intake of the commonest cassava food, and 1.64 (0.56 to 5.09) for concentration of thiocyanate in plasma. The concentration of thiols was less than the reference limits in two controls, but in none of the cases. The latency of P100 was prolonged in 20 cases (69%) compared with 14 controls (42%) (p<0.05). CONCLUSIONS: The incidence of ataxic polyneuropathy is high in Ososa, Nigeria, but the intake of cassava foods, exposure to cyanide, and levels of thiols, are not related to the occurrence. These findings do not suggest that cyanide is the cause of endemic ataxic polyneuropathy.

Adolescent↗
PubMed1996

Cyanide degradation by an Escherichia coli strain.

Chemical formation of a glucose-cyanide complex was necessary for metabolic degradation of cyanide at concentrations up to 50.0 mg/L by a strain of Escherichia coli isolated from gold extraction circuit liquids. Ammonia accumulating during the culture log phase as the sole nitrogen by-product was further utilized for bacterial growth. Washed (intact) cells, harvested at different periods of bacterial growth on cyanide, consumed oxygen in presence of cyanide. These findings suggest that metabolism of cyanide involved a dioxygenase enzyme that converted cyanide directly to ammonia, without the formation of cyanate.

Ammonia↗
PubMed1993

Central and spinal effects of sodium cyanide on respiratory activity.

The pharmacological actions of cyanide on respiratory activity have been known for some time and are attributed mainly to effects on peripheral chemoreceptors. In the studies reported here, we have examined the acute central effects of cyanide when applied topically to the ventral surface of the medulla (VMS) and when administered into the spinal intrathecal space at the C5-T3 level on activities of the phrenic nerve, diaphragm, parasternal intercostal, triangularis sterni, and transversus abdominis muscles. Topical application of 10-100 micrograms (10 microliters of 1-10 mg/ml) cyanide to the intermediate area of the VMS decreased respiratory activity by > 50%, and expiratory muscles were more sensitive to inhibition than inspiratory muscles. The onset of depression of phrenic nerve or respiratory muscle activity occurred within 20 s of administration, and the effects reversed after washout. In contrast, intrathecal administration of cyanide in doses of 10-100 micrograms (100 microliters of 0.1-1 mg/ml) increased electrical activity of the respiratory muscles. Diaphragm activity changed from 17 +/- 2 to 42 +/- 8 (SE) units (P < 0.01), parasternal intercostal activity increased from 18 +/- 3 to 46 +/- 9 units (P < 0.01), and expiratory activity of the chest wall and abdominal muscles increased from 9 +/- 2 to 39 +/- 10 units (P < 0.05). Both topical application on the VMS and intrathecal administration of cyanide caused an increase in arterial blood pressure and a slight insignificant acceleration of heart rate. These data suggest that cyanide acting on the VMS causes respiratory depression and enhancement of sympathetic outflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed2004

Cyanide poisoning and its treatment.

Cyanide is both widely available and easily accessible throughout the world. Although the compound is not frequently encountered, it has been used as a poison and contaminant in the past and is a potential terrorist agent. Cyanide has the ability to cause significant social disruption and demands special attention to public health preparedness. It can be obtained from a variety of sources, including industrial, medical, and even common household products. Another frequently encountered source of cyanide exposure is residential fires. Exposure to high concentrations of the chemical can result in death within seconds to minutes. Long-term effects from cyanide exposure can cause significant morbidity. The only treatment for cyanide toxicity approved for use in the United States is a kit consisting of amyl nitrite, sodium nitrite, and sodium thiosulfate. Future research aims to find a faster-acting, more effective, and better tolerated treatment for cyanide toxicity.

Antidotes↗
PubMed2004

Cyanide reaction with ninhydrin: elucidation of reaction and interference mechanisms.

A new sensitive spectrophotometric method has recently been developed for the trace determination of cyanide with ninhydrin. Cyanide ion was supposed to act as a specific base catalyst. Nevertheless, this paper demonstrates that the reported assay is based on a novel reaction of cyanide with 2,2-dihydroxy-1,3-indanedione, which affords purple or blue colored salts of 2-cyano-1,2,3-trihydroxy-2H indene. Hydrindantin is merely an intermediary of the reaction. The formation of a stable and isolable ninhydrin-cyanide compound has been confirmed by its preparation in crystalline form. Also, it is thoroughly characterized by elemental as well as MS, IR, UV/VIS and 1H NMR analyses. The Ruhemann's sequence of reactions of cyanide with ninhydrin has been reconsidered and an adequate mechanism of the reaction is proposed. As a consequence, the interference of oxidizers as well as copper, silver and mercury ions with the cyanide determination has been elucidated.

Cyanides↗
PubMedDate not supplied

Effects of thiocyanate on the formation of free cyanide during chlorination and ultraviolet disinfection of publicly owned treatment works secondary effluent.

Cyanide has been detected in effluent of some publicly owned treatment works (POTWs) at levels exceeding influent concentration. Thiocyanate (SCN-) is a cyanide-related compound encountered in most POTW influents and may be decomposed to free cyanide (CN-) under some circumstances. Effects of SCN- on the formation of cyanide during chlorination and UV disinfection were studied through a laboratory study with synthetic solutions and POTW secondary effluent. Results indicated that CN- was detected in SCN- solutions after chlorination in which the chlorine dose or reaction time was not sufficient to destroy SCN-completely, thus ensuring no residual chlorine to destroy any CN-produced. It was also found that SCN can be broken down to yield cyanide by UV irradiation. In addition, SCN- was observed to cause significant positive error in the conventional total cyanide analysis technique involving acidic distillation and colorimetric measurement when nitrate was present in the sample.

Chemistry Techniques, Analytical↗
PubMedDate not supplied

Dietary cyanide and tropical malnutrition diabetes.

Two categories of diabetes are recognized in the temperate zone--ketosis-prone diabetes requiring insulin and diabetes not requiring insulin. Another unique type of diabetes occurs in the tropics. It has two forms, both different from either form of temperate zone diabetes. Type J and pancreatic diabetes are both characterized by youth onset, antecedent malnutrition, substantial insulin requirement, and resistance to ketosis. In the tropical countries where they are found, both forms are associated with specific dietary practices, including a nutritionally marginal protein intake. The close association with low protein intake distinguishes this form of diabetes from that occurring in North America, Europe, and Oceania. The geographic distribution of malnutrition diabetes, in addition to being limited to the tropics, coincides regularly with the consumption of tapioca (cassava) or other foods that contain cyanide-yielding substances. Ingested cyanide is normally detoxified, principally, by conversion to thiocyanate. This detoxification requires sulfur, derived principally from amino acid sources. Studies in the rat indicate a remarkable ability to detoxify ingested cyanide, a reduction in urinary thiocyanate excretion when protein intake is lowered (especially during growth), production of marked hyperglycemia by either oral or parenteral cyanide, and the development of cyanosis and epidermal changes when there is prolonged exposure to cyanide. Both the association of malnutrition diabetes with food cyanogens and our laboratory observations support a role for cyanide in its pathogenesis.

Adolescent↗
PubMed1993

Potassium cyanide protects Escherichia coli from complement killing by the inhibition of C3 convertase activity.

The exact mechanism by which deposited C5b-9 complexes kill Gram-negative bacteria is unclear. It has been proposed that during complement activation the membrane attack complex triggers an energy dependent process in Gram-negative bacteria that mediates destruction of the inner membrane. This observation in part resulted from the survival of Gram-negative bacteria that were incubated with an uncoupler (DNP) or an inhibitor (KCN) of oxidative phosphorylation during complement activation. In a reexamination of this issue we employed potassium cyanide (KCN) to block energy dependent pathways and observed a dose dependent inhibition of C9 uptake on E. coli J5 during serum incubation, suggesting that cyanide was interfering with complement activation. To verify the effect on complement activation we chose specifically to study the effects of KCN on the C3 convertase of the classical pathway. Sensitized sheep erythrocytes were employed as our model system. This system allowed us to construct a series of stable intermediates that were used to test the effect of cyanide on the formation and activity of precursors of the classical pathway C3 convertase. The data illustrate that the concentrations of potassium cyanide that inhibit complement killing of J5 also inhibit C3 convertase activity on sensitized sheep erythrocytes. The results of this study refute the principal observation made by other investigators, that potassium cyanide protects bacteria from complement killing by inhibiting bacterial energy dependent pathways that spark inner membrane destruction. A better scenario is that the organisms survive because cyanide inhibits complement activation.

Animals↗