Cyanide endogenous

Methaemoglobin forming compounds should be used cautiously in victims suffering from concurrent carbon monoxide poisoning or hypoxia. The second approach calls for provision of additional sulfur groups to enhance the detoxification of cyanide and thiocyanate by endogenous rhodanese this comes about by giving sodium thiosulphate. 

While cyanide inhibition of cytochrome c oxidase may not account for the full spectrum of toxicity in CS exposure, cyanide toxicity may include an array of biochemical interactions (Way, 1984). These include lipid peroxidation (Johnson et al, 1987), cyanide release of endogenous opioids to cause respiratory paralysis (Leung et al, 1986), disruption of neuronal calcium homeostasis (Johnson et al, 1986), and phospholipids hydrolysis (Sakaida and Farber,... 

Cyanide also causes endogenous catecholamine release (Kanthasamyeta/., 1991 Kawada eta/., 2000 Schomiget a/., 1995 Inoue et al, 1998). Inoue et al (1998) also point out that cyanide-produced depolarization increases intracellular calcium due to the suppression of the potassium channels and activation of the voltage-dependent calcium channel. Anoxia induces suppression of the sodium pump and activates cation channels due to the decrease in ATP. A further consequence of the presence of cyanide in the tissue is inhibition of the Na+/Ca + exchanger (NCX) (Ju and Allen, 2005). NCX is important for the pacemaker currents. Metabolic inhibition of NCX reduces the firing rate of pacemaker cells. 

Borowitz, J., Gunasekar, P., Isom, G. (1997). Hydrogen cyanide generation by mu opiate receptor activation Possible neuromodulatory role of endogenous cyanide. Brain Research, 768, 294-300. 

Tadic, V. (1992). The possible role of the system of endogenous opioids in the mechanism of cyanide toxicity. Acta Veterinaria (Beograd), 42, 43—52. 

For galactose (50 mg/100 ml) added to Somogyi filtrates, ten replicate analyses showed (CIO) a mean recovery of 100.2 with a standard deviation of 1.2. For endogenous glucose, ten analyses gave a mean recovery of 83.6 mg/100 ml (standard deviation, 1.3) compared with the value of 86.6 mg/100 ml when determined by an automated ferri-cyanide method. Recoveries of added sugars are shown in Tables 9 and 10. 

Borowitz, Isom, and Baskin describe key pathologic sequelae to acute and chronic exposure to cyanide. They provide exposure and risk assessment, with emphasis on the effects of cyanide on the neural tissue. These effects are primarily characterized as effects of cyanide on the metabohsm of neurons, cyanide and oxidative stress in neuronal cells, cyanide-induced hyperpolarization, and neuronal activation by cyanide, processes which implicate abnormal sodium channel function in cyanide-induced neuronal damage. Endogenous generation of cyanide in neuronal tissue is also postulated as a causal mechanism in disease. Problems in metabolism of cyanide leading to chronic, low-level exposure are described and discussed. 

B. divergens) have been reported to contain an endogenous superoxide dismutase that is cyanide-insensitive and inhibited by H2O2 indicating that iron is the cofactor metal... 

Some drugs are detoxified by conjugation with glucuronic acid or sulfate before elimination from the body, and the availability of the endogenous cosubstrates for conjugation may limit the rate of elimination such is the case in the detoxication of acetaminophen. Repletion of these compounds will provide an additional mechanism to treat poisoning. For instance, detoxication of cyanide by conversion to thiocyanate can be accelerated by the administration of thiosulfate. 

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