The in Vivo Inactivation by Cyanide of Brain Cytochrome Oxidase and Its Effect on Glycolysis and on the High Energy Phosphorus Compounds in Brain

Albaum, Harry G.; Tepperman, Jay; Bodansky, Oscar

doi:10.1016/s0021-9258(18)43046-3

Cited by 86 publications

(14 citation statements)

References 6 publications

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“…Treatment of cyanide correlated with an anoxic state, resulting in a shift from aerobic to anaerobic metabolism, thus supporting a model in which cyanide inactivates CCOx by interfering with the utilization of molecular oxygen [22].…”

Section: Cyanide As An Inhibitor Of Mitochondrial Respiration and As A Cytotoxic Agentsupporting

confidence: 57%

“…developing/proliferating cells, neurons, cardiac myocytes). Indeed, in vivo or ex vivo studies show that ATP and high-energy phosphate content of the tissues decrease rapidly and precipitously after systemic exposure to cyanide [43][44][45][46][47][48][49] and the inhibition of mitochondrial Complex IV is well detectable in various tissues ex vivo [22,48,[50][51][52]. In line with the inhibition of mitochondrial function, tissues exposed to cyanide lose their ability to extract oxygen, even in the presence of adequate blood flow [53,54], a phenomenon called "cytotoxic hypoxia".…”

Section: Accepted Articlementioning

confidence: 99%

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The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

Zuhra

Szabó

2021

The FEBS Journal

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Section: Cyanide As An Inhibitor Of Mitochondrial Respiration and As A Cytotoxic Agentsupporting

confidence: 57%

Section: Accepted Articlementioning

confidence: 99%

The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

Zuhra

Szabó

2021

The FEBS Journal

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“…Acetonitrile used as a solvent for the active ingredients in this research was inorganic cyanide, which reacted with Fe 3+ of cytochrome oxidase in mitochondria and ensured cellular respiration by oxygen reduction [36]. Formaldehyde and formic acid have been postulated as being products of acetonitrile metabolism [44].…”

Section: Monitoring Exhaled Co 2 Concentrationmentioning

confidence: 99%

“…Prallethrin and d-phenothrin were purchased from Sigma Aldrich with catalogue number of prallethrin 32,917 and d-phenothrin 36,193. In this research, two doses of prallethrin and d-phenothrin mixtures comprised the lower and higher doses.…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

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The effects of particulate matters inhalation exposures of prallethrin and d-phenothrin mixture in mice (Mus musculus) against exhaled carbon dioxide concentration

2019

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Particulate matter (PM) inhalation exposure affects exhaled CO 2 concentration. Such exhaled CO 2 refers to ventilation and perfusion of the cardiorespiratory system, the analysis of which is painless, non-invasive and simple to perform. This study examined the effect of prallethrin and d-phenothrin inhalation exposure on exhaled CO 2 in mice using a simple method. Prallethrin and d-phenothrin were administered in male mice (Mus musculus) in a series of repeated inhalation exposures of lower and higher doses for 60 days. The lower dose was a mixture of 0.000141 mg/L prallethrin and 0.104 mg/L d-phenothrin, while the higher dose was a mixture of 0.00141 mg/L prallethrin and 1.04 mg/L d-phenothrin. The lower dose was based on a NOAEL value of prallethrin and d-phenothrin of 28 days exposure, while the higher one was ten times of the lower dose concentration. CO 2 concentration was measured by means of the passage through NaOH 0.1 N, titrated by HCl 0.1 N. PMs were generated by the process of producing bubbles, inserted into the chamber containing mice. Mice were divided into four groups, namely: negative control (NC), positive control (PC), and lower-and higher-dose treatment groups, with three replicates for each group. Statistical difference analyses were observed in body weight and exhaled CO 2 concentration between negative control and treatment groups, nevertheless, they did not differ significantly between the control and the treatment (lower and higher dose) groups. This study suggests that exhaled CO 2 and body weight are not specific biomarkers to observe PMs inhalation exposure with respect to prallethrin and d-phenothrin mixtures.

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Mechanism of action of sodium cyanide on rat diaphragm muscle

Adler¹,

Lebeda

Kauffman

et al. 1999

J. Appl. Toxicol.

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The effects of sodium cyanide (NaCN) were investigated on the contractile and electrophysiological properties of rat diaphragm muscles in vitro. Sodium cyanide (0.1–1.0 mM) produced an initial potentiation of directly elicited twitch tensions, followed by a slow progressive depression. The potentiation and depression were both dependent on the NaCN concentration and stimulation frequency. Muscles exposed to NaCN exhibited marked reductions of creatine phosphate concentration, but ATP levels were not significantly lowered. Sodium cyanide had no effect on the resting potential, input resistance or action potential, indicating that the toxicity of the metabolic inhibitor is not mediated by alterations of membrane excitability or passive electrical properties. Sodium cyanide reduced the amplitude of contractures elicited by 70 mM K2SO4, suggesting that the actions of NaCN cannot be explained by a failure of action potentials to propagate across the muscle surface or within t‐tubular membranes. Sodium cyanide suppressed the first phase of the caffeine contracture, an observation consistent with an impaired release of, or reduced sensitivity to, sarcoplasmic reticular Ca2+, but did not alter the amplitude of the second phase, which represents rigor following ATP depletion. These results, in conjunction with those of previous studies, suggest that the depression in muscle tension following exposure to NaCN may result from alterations in Ca2+ homeostasis, intracellular acidosis or from accumulation of one or more products of phosphocreatine breakdown. Copyright © 1999 John Wiley & Sons, Ltd.

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The in Vivo Inactivation by Cyanide of Brain Cytochrome Oxidase and Its Effect on Glycolysis and on the High Energy Phosphorus Compounds in Brain

Cited by 86 publications

References 6 publications

The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

The effects of particulate matters inhalation exposures of prallethrin and d-phenothrin mixture in mice (Mus musculus) against exhaled carbon dioxide concentration

Mechanism of action of sodium cyanide on rat diaphragm muscle

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