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PubMed2004

[Two suicide fatalities from sodium cyanide ingestion: differences in blood biochemistry].

We report a case of two suicide fatalities from sodium cyanide ingestion, which showed differences in pathology and blood biochemistry. The victims were a married couple in their 70 years of age, owners of a gilding factory. They were found dead in their bedroom by a family member. Suicide notes and sodium cyanide powder were found in the room. Autopsy revealed eroded gastric mucosae in both victims. In the male, the stomach showed a previous postoperative state of partial resection, and the lungs were more congested and edematous in the male than in the female. In both victims, cyanide was detected in the blood at markedly high concentrations. In postmortem blood biochemistry, a marked elevation of cardiac troponin T, I and CK-MB was observed in the peripheral blood of the male, whereas there was only a mild elevation in the female. In the male, erythropoietin was also markedly elevated. These observations suggested a difference in the dying process following sodium cyanide ingestion between the victims; survival time may have been longer in the male than the female. The absorption of cyanide may have been a contributory factor to the difference.

Aged↗
PubMed2006

[Effects of drought stress on cyanide-resistant respiration and metabolism of reactive oxygen in wheat seedling].

The changes in cyanide-resistant respiration and metabolism of active oxygen species in drought-sensitive and drought-resistant wheat seedlings under water stress were studied. In general, drought stress decreased the level of cyanide-resistant respiration and AOX1 mRNA content in wheat seedling leaves. But the drought-resistant cultivars, which had much higher level of cyanide-resistant respiration and AOX1 mRNA content than the drought-sensitive ones, presented an ability to adapt to mild drought stress. Under drought stress, the drought-sensitive wheat seedling leaves had higher O(-.)(2) and H(2)O(2) contents, but lower SOD, POX and CAT activities than drought-resistant cultivars. We guessed that severe drought stress could break down the balance between active oxygen species and cyanide-resistant respiration. However, cyanide-resistant respiration still could participate in the drought-resistance by lowering the level of active oxygen species besides by other mechanism.

Blotting, Northern↗
PubMed1991

Validity of salivary thiocyanate as an indicator of cyanide exposure from smoking.

The purpose of this study was to evaluate the validity of salivary thiocyanate as an indicator of cyanide exposure from smoking. The salivary thiocyanate level showed wide variation, and the largest source of thiocyanate was hydrogen cyanide from cigarette smoke. Hydrogen cyanide in the mainstream of cigarette smoke was as high as 40-70 ppm, which is beyond the threshold limit value for occupational health (10 ppm). The hydrogen cyanide level in the sidestream smoke was lower less than 5 ppm. Thus the amount of cyanide intake was larger in active smokers than in passive ones. The correlation between the thiocyanate level in saliva and plasma was statistically significant. Thiocyanate levels in both plasma and saliva increased with the amount of cigarette smoke, and the discriminant powers (smoker versus non smoker) of thiocyanate levels in both plasma and saliva were quite similar. The smoker/non smoker ratio for salivary thiocyanate was 3.04 and that of plasma thiocyanate was 1.73. The result indicated that smoking status could be reflected more by the thiocyanate level in saliva than in plasma. The biological half life of salivary thiocyanate was estimated to be as long as 9.5 days from the changes salivary thiocyanate after stopping smoking. From the results of this study, it was concluded that salivary thiocyanate was a suitable indicator of habitual smoking exposure.

Humans↗
PubMed1992

Cooperative cyanide dissociation from ferrous hemoglobin.

Rapid reduction of cyano-met hemoglobin (Hb+CN-) leads to the formation of an intermediate species, the cyanide derivative of ferrous hemoglobin, which dissociates to unliganded hemoglobin because of the extremely low affinity of the ligand for the ferrous heme iron. The properties of the intermediate were studied by transient spectroscopy in human hemoglobin and its isolated alpha and beta chains, in the presence and absence of CO. When mixing with dithionite, the time courses of reduction of the heme iron and dissociation of cyanide overlap considerably; addition to the reaction mixture of the redox indicator methyl viologen considerably increases the rate of reduction and allows unequivocal determination of the spectroscopic and kinetic properties of the intermediate. The results show that (i) the dissociation of cyanide from the isolated alpha and beta chains (as well as the (alpha CO)2(beta + CN-)2 hybrid) is a simple process; (ii) the two chains display similar rate parameters, but show spectroscopic inequivalence, both in the Soret and the visible regions; (iii) cooperative effects are shown to control the rate of dissociation of cyanide from hemoglobin, similarly to what happens for oxygen; and (iv) allosteric effectors (typically inositol hexaphosphate) increase the overall rate of dissociation by stabilization of the T state. We have, therefore, shown for the first time that the dissociation of cyanide from ferrous hemoglobin is controlled by the quaternary state, thereby adding one more ligand to the analysis of the structure-function relationships in hemoglobin.

Cyanides↗
PubMed1991

Dietary cyanide effect on performance and serum testosterone of growing male pigs.

48 growing male pigs were fed cyanide in different doses (0, 250, and 500 mg/kg) and its effect was determined on their growth performance and serum testosterone content. The rations were balanced as regards the energy and protein content. Increased cyanide additions had a significant influence on the weight gain, feed intake, as well as the feed and protein efficiency of the animals. Examination of the pancreas showed histological changes following high cyanide additions. Dietary cyanide levels of 500 mg/kg did significantly affect the serum testosterone level. A non-significant correlation (r = -0.22) existed between the daily cyanide intake and serum testosterone.

Animals↗
PubMed1989

[A study of the mechanism of cyanide resistant oxidation of succinate from rat liver mitochondria in the presence of menadione].

Two operation regimes of the electron transport system were found in rat liver mitochondria during the cyanide-resistant succinate oxidation catalyzed by menadione. Under isotonic conditions, the mitochondria were found to contain two electron transport components, one of which was sensitive to mucidin, whereas the other one was inhibited by antimycin A. Both electron transport components were inhibited by thenoyltrifluoroacetone (TTFA). In hypotonic media, the polyenzymatic respiratory complex of mitochondria underwent transformations. In this case the electron transport during the cyanide-resistant succinate oxidation was insensitive to mucidin and antimycin A and was suppressed only by TTFA. Some experimental evidence in favour of pathways of electron transfer under different regimes of mitochondrial function was obtained. It was supposed that in isotonic incubation media the cyanide-resistant respiration is mainly due to menadione reduction in two points of the Q-cycle, i.e., in the region of the "i" center and in the "o" center. Under hypotonic conditions, the main electron flux to menadione occurs only via the Q-cycle "i" center. The observed relatively slow reduction of cytochromes b and ci+c plays an insignificant role in the cyanide-resistant respiration. It was shown that the ability of menadione to stimulate the cyanide-resistant respiration is correlated with a higher polarity of this compound as compared with CoQ2 and endogenous CoQ10 of mitochondria. The role of the polyisoprenoid substituent in CoQ10 as a structural component providing for the specificity of interaction with mitochondrial respiratory chain carriers is discussed.

Alkenes↗
PubMed1988

Cyanide and thiocyanate blood levels in patients with renal failure or respiratory disease.

Whole blood cyanide and plasma thiocyanate were measured by a headspace gas chromatographic method and a colorimetric method, respectively, in 16 healthy subjects, in 10 patients with respiratory disease and in 12 patients on chronic dialysis for renal failure. In healthy subjects, whole blood cyanide and plasma thiocyanate concentrations were significantly higher in smokers (1.8 +/- 0.4 mumol/l; 206 +/- 74 mumol/l) than in non-smokers (0.8 +/- 0.4 mumol/l; 74 +/- 19 mumol/l). In renal failure patients on hemodialysis, no difference was noted in cyanide levels (0.6 +/- 0.4 mumol/l), but there was a significant increase in plasma thiocyanate levels during the interdialysis period (62 +/- 24 mumol/l; 91 +/- 24 mumol/l). No difference in cyanide and thiocyanate levels of patients with respiratory disease was seen, in agreement with a weak pulmonary elimination of cyanide.

Cyanides↗
PubMedDate not supplied

Cyanide, protein and iodine interaction in the performance and metabolism of rats.

Performance and metabolic traits were measured in sixty-four growing rats fed on varying levels of dietary cyanide, protein and iodine. The presence of cyanide in the diets caused a non-significant reduction in both feed consumption and growth rate. Moreover, on protein deficient diets, the lowest body weight gain was obtained in the animals with 750 ppm cyanide. Iodine deficiency did not have any marked influence on performance. Dietary cyanide significantly increased serum and urinary thiocyanate concentration while iodine deficiency caused significant reductions in serum protein bound iodine (PBI). Interactions of protein deficiency and dietary cyanide also significantly reduced serum thiocyanate concentrations, while interactions of the three dietary variables significantly reduced kidney protein content.

Animals↗
PubMed1984

[Cyanide poisoning. Priority to symptomatic treatment. 25 cases].

A retrospective study of 25 cases of cyanide poisoning has brought to light the following points: cardiorespiratory arrests are frequent (7/25) and often inaugural; in severe intoxications (7/25), deep metabolic acidosis is the rule, and cyanide poisoning should always be suspected in cases of coma with severe acidosis; mild intoxications are frequently symptomless. Anxiety and agitation should not be considered as evidence of cyanide poisoning; they are merely due to fear in most cases. The present treatment of acute cyanide poisoning relies basically on symptomatic measures: sodium bicarbonate, cardiac massage and, above all, assisted ventilation with 100% oxygen. Our experience does not support the concept of a lethal cyanide blood level when patients can rapidly be transferred by a medical team to an intensive care unit. Survival depends more on prompt medical care than on the accessibility to sophisticated antidotes.

Acidosis↗
PubMed1980

Cyanide binding to the cytochrome c ferric heme octapeptide. A model for anion binding to the active site of high spin ferric heme proteins.

Equilibrium constants for the binding of cyanide to the ferric heme c octapeptide in 20% ethylene glycol, 50% buffer were measured spectrophotometrically. The equilibrium constant for cyanide binding at 20 degrees C and pH 7.4 is 3.47 X 10(7), which is approximately 15-fold lower than that observed for cyanide binding to methemoglobin or metmyoglobin. Equilibrium constants at several temperatures exhibited an apparent van't Hoff relationship, yielding thermodynamic values of delta H degrees = -79,000 J/mol (-18,900 cal/mol) and delta S degrees = J/degrees K mol (-30.1 e.u.). Comparison of the ratio of equilibrium constants for cyanide ligation to methemoglobin the heme octapeptide with the ratio of equilibrium constants for azide ligation to methemoglobin and the heme octapeptide suggests that cyanide binding to the methemoproteins is much smaller than expected by comparison to azide binding. The differences in the ratios, the thermodynamic values, and the preferred binding geometries suggest that CN- ligation, like CO ligation, is sterically hindered. A comparison of these ratios to similar ratios for CO, O2, and NO binding suggests that the Fe-CN bond angle is less subject to distortion than the Fe-CO bond and/or additional binding interactions contribute to N3- but not to CN-binding to the protein.

Animals↗
PubMed1984

The effect of naftidrofuryl on cyanide-induced hypoxic damage to glucose and energy metabolism in brain cortex of rats.

Increasing life expectancy increases diseases of old age. Dementia is a highly age-related brain disease in which the metabolic rates of oxygen and glucose are predominantly disturbed. However, related changes in metabolism at the molecular level are rather little known. Knowledge on pharmacotherapeutic modification of the metabolic variations in the brains of demented people is also scanty. Since the vascular type of primary dementia is found to be associated with metabolic variations which resemble that of a cerebral hypoxia, hypoxic brain damage was produced by means of a sublethal dosage of cyanide in two-year-old rats. The cyanide-induced damage in brain metabolism was characterized by an increase of the tricarboxylic acid cycle intermediates succinate, fumarate and malate. This indicates disturbances of NAD+- and FAD+-dependent redox reactions also including pyruvate oxidation. Lactate production was found to be increased, and creatine phosphate formation reduced. Application of 3 mg/kg naftidrofuryl after cyanide damage produced a normalizing effect on the cyanide-induced changes in glucose and energy metabolism of brain cortex of rats. The tentative conclusion may thus be drawn that naftidrofuryl may have a beneficial effect on cyanide-induced hypoxic brain damage. Whether this drug might be useful in other brain hypoxic conditions remains to be investigated.

Animals↗
PubMedDate not supplied

[Cyanide-resistant respiration of bacteria and its relation to metabolite oversynthesis].

The phenomenon of cyanide-resistant respiration was studied in bacteria as well as its relation to the oversynthesis of metabolites. Cyanide-resistant respiration was shown to be common of aerobic and facultative anaerobic bacteria. The resistance of respiration to cyanide was observed when the growth of a microbial culture was inhibited or ceased entirely, provided the culture lacked the oversynthesis of metabolites. When a culture was capable of metabolites oversynthesis under such conditions, cyanide-resistant respiration (if any) declined. Therefore, there is a competition between metabolites oversynthesis and cyanide-resistant respiration, which is typical of many microorganisms.

Aerobiosis↗
PubMedDate not supplied

[Effect of sulfur, copper, and iron deficiency on the development of cyanide resistant respiration and the cytochrome composition of Pseudomonas aeruginosa].

The effect of deficiency in sulfur, copper and iron in the growth medium on cyanide resistant respiration and cytochrome composition was studied in Pseudomonas aeruginosa and Candida lipolytica. It has been shown that: cyanide resistant respiration was observed at the stationary growth phase when the two microorganisms were cultivated in a complete medium; this respiration was detected already at the phase of decelerated growth in the case of copper deficiency; iron deficiency inhibited cyanide resistant respiration in the bacterium but stimulated its appearance in the yeast; sulfur deficiency inhibited the manifestation of cyanide resistant respiration in the both microorganisms; limitation of the bacterial growth with iron resulted in the accumulation of an iron complex (identical to pyoverdin in its spectral characteristics) in the cultural broth; the deficiency of sulfur, copper and iron inhibited the synthesis of all cytochromes in the bacterium; copper deficiency inhibited only the synthesis of a + a3 in the yeast; iron deficiency inhibited the synthesis of all cytochromes in the yeast; sulfur deficiency had virtually no effect on the content of cytochromes in the yeast. A possible nature of cyanide resistant oxidases in these microorganisms is discussed.

Candida↗
PubMed1981

[Cause of the activity loss of the alternative pathway of electron transport in cyanide-resistant mitochondria of the yeast Candida lipolytica].

The cause of the activity loss of alternative pathway of electron transport in mitochondria of the yeast Candida lipolytica has been investigated. Incubation of cyanide-resistant mitochondria at 25 degrees was shown to cause the loss by mitochondria of their ability to oxidize substrates in the presence of 1 mM cyanide. This suggests that in the course of incubation the alternative pathway loses its activity. Repeated washing of mitochondria with a solution containing 2,5 mM EDTA inhibits, while Ca2+, Mn2+, Cu2+ and Zn2+ (but not Sr2+) enhance the process of the activity loss of the alternative pathway. The loss of the cyanide-resistant respiration is also observed during incubation of mitochondria in the presence of phospholipases A, C and D or lysolecithin. In all cases studied the reactivation of the cyanide-resistant respiration of mitochondria is attained by addition of azolectin. The loss of cyanide-resistant respiration is accompanied by the activity reduction of the main respiratory chain, which is restored by addition of cytochrome c and Mg2+. These data indicate that the activity loss of the alternative pathway is not related to inactivation of any components in the alternative pathway itself or in the main respiratory chain. The most probable cause of the activity loss in the destruction of reducing equivalents in the alternative pathway of a donor as a result of a break of the structural entity of the internal membrane of mitochondria due to the detersive action of the phospholipid lysoforms produced either by endogenic or exogenic phospholipases.

Candida↗
PubMed1994

Probing the oxygen binding site of cytochrome c oxidase by cyanide.

Cyanide binding to cytochrome c oxidase has been investigated by sequential mixing and rapid scan stopped flow spectroscopy. Double mixing experiments confirm earlier reports that cyanide binds rapidly to partially reduced enzyme species formed in turnover. The absorbance/time/wavelength matrices, captured during the onset of cyanide inhibition of cytochrome c oxidase by rapid scan stopped flow, were analyzed by singular value decomposition and the spectral contributions of the chromophores separated. Examination of the time courses and amplitudes of the spectral signals provide evidence that entry of a single (1-1.3) electron into the enzyme is sufficient to trigger rapid cyanide binding. This electron resides predominantly on the cytochrome a/CuA pair in the inhibited enzyme. In addition, although cytochrome a3 remains oxidized, it does not appear to be the site for the initial inhibitory binding of cyanide. Our data suggest that CuB2+ is the initial binding site.

Cyanides↗
PubMed1993

Cyanide toxicity. Agency for Toxic Substances and Disease Registry.

Cyanide is one of the most rapidly acting poisons. Cyanide poisoning is a hazard that may accompany enclosed-space fires, and its occurrence in persons with smoke-inhalation injuries may be underestimated. Acute cyanide exposure primarily causes central nervous system, cardiovascular and respiratory effects. Thyroid function abnormalities have been noted in persons chronically exposed to cyanide. Initial symptoms may be nonspecific. Death may occur in seconds after acute inhalation of hydrogen cyanide.

Cyanides↗
PubMedDate not supplied

A retrospective study of sodium nitroprusside use and assessment of the potential risk of cyanide poisoning.

Sodium nitroprusside (SNP) is an effective vasodilator but is potentially dangerous due to its cyanide content. Infusion rates above 2 micrograms/kg/minute may cause cyanide to accumulate to toxic concentrations in critically ill patients. Coadministration of thiosulfate with SNP effectively and safely prevents cyanide toxicity. This study determined if patients at our institution were treated with SNP infusion rates that could cause cyanide toxicity and whether those patients were administered thiosulfate. We reviewed the charts of 36 critically ill patients treated with SNP during the previous 12 months. In 72% of patients the SNP infusion rates were above 2 micrograms/kg/minute. In 47% the rates were greater than 2 micrograms/kg/minute for 6 hours or more, and in 20% they were greater than 5 micrograms/kg/minute for up to 11 hours. None of the patients was administered thiosulfate. In a significant number of patients the infusion rates of SNP potentially exposed them to significant risk of cyanide toxicity including death.

Adolescent↗
PubMed1996

Cyanide-induced neurotoxicity involves nitric oxide and reactive oxygen species generation after N-methyl-D-aspartate receptor activation.

To study oxidative mechanisms in cyanide toxicity, cyanide-induced generation of intracellular oxidant species was determined by microfluorescence in cerebellar granule cells loaded with the oxidant-sensitive fluorescence dye 2,7-dichlorofluorescin. KCN produced a concentration-dependent (25-200 microM) generation of intracellular oxidant species that was blocked by N-methyl-D-aspartate receptor antagonists (MK-801 or AP5) or by removal of extracellular Ca++ from the incubation medium. To determine the relative contribution of NO and reactive oxygen species (ROS) to the increase of cellular fluorescence after KCN, a selective inhibitor of nitric oxide synthase, a NO scavenger and enzymes that metabolize ROS were added to the incubation medium. Interference with the nitric oxide system (reduced hemoglobin as a NO scavenger or [N(G)-nitro-L-arginine methyl ester [L-NAME] reduced fluorescence by 50%). Addition of enzymes that metabolize peroxide (catalase or superoxide dismutase [SOD]) also reduced fluorescence by nearly 50%. Combination of SOD with hemoglobin or L-NAME provided additional attenuation of the fluorescence and it was concluded that both NO and ROS are generated concurrently after KCN. Furthermore a correlation was observed between NO and ROS formation and levels of malonaldehyde (MDA), a marker of lipid peroxidation. Pretreatment with MK-801 blocked KCN-induced MDA formation, whereas L-NAME partially diminished MDA production. Treatment with a combination of SOD/catalase and L-NAME blocked the KCN-induced lipid peroxidation. In cytotoxicity studies cyanide-induced cell death was blocked by MK-801, whereas partial attenuation was produced by L-NAME; SOD/catalase treatments did not protect the cells. However, significant protection from cyanide-induced cytotoxicity was observed when L-NAME was combined with SOD/catalase. It is concluded that cyanide activates N-methyl-D-aspartate receptors to simultaneously generate both NO and ROS, which may lead to formation of the cytotoxic peroxynitrite anion.

Animals↗