Thiosulfate oxidase

No drug, including sodium thiosulfate, should be administered without clear indication. Like all other drugs, sodium thiosulfate is also not without its own toxicity. Sodium thiosulfate can even be converted into cyanide by the enzyme thiosulfate oxidase (Goldstein and Reiders, 1951), which is the reason why its overzealous use in cases of cyanide poisoning can lead to recurrence of symptoms. 

Biochemically, manganese is considered an essential trace element, participating in a number of hiomolecules superoxide dismutase (Mn-SOD), catalase, Mn-ribonucleotide reductase, Mn-peroxidase, ligninase, the o>ygen-evolving centre (OEC) of photosystem ii (PS-ii), and Mn-thiosulfate oxidase. The enzymes mechanisms are very diverse and include oxo-atom transfer (four-electron oxidation of water to diojygen in PS-ii, extradiol dioxygenase), electron transfer (SOD, catalase), reduction of ribonucleotides to water and deoxyribonucleotides and oxidation of thiosulfate to sulfate. ... 

HCN is a systemic poison toxicity is due to inhibition of cytochrome oxidase, which prevents cellular utilization of oxygen. Inhibition of the terminal step of electron transport in cells of the brain results in loss of consciousness, respiratory arrest, and ultimately, death. Stimulation of the chemoreceptors of the carotid and aortic bodies produces a brief period of hyperpnea cardiac irregularities may also occur. The biochemical mechanisms of cyanide action are the same for all mammalian species. HCN is metabolized by the enzyme rhodanese which catalyzes the transfer of sulfur from thiosulfate to cyanide to yield the relatively nontoxic thiocyanate. 

Thiosulfate cyanide sulfurtransferase symmetry in 78 TTiiouridine 234 Three-dimensional structures of aconitase 689 adenylate kinase 655 aldehyde oxido-reductase 891 D-amino acid oxidase 791 a-amylase, pancreatic 607 aspartate aminotransferase 57,135 catalytic intermediates 752 aspartate carbamyltransferase 348 aspartate chemoreceptor 562 bacteriophage P22 66 cadherin 408 calmodulin 317 carbonic acid anhydrase I 679 carboxypeptidase A 64 catalase 853 cholera toxin 333, 546 chymotrypsin 611 citrate synthase 702, 703 cutinase 134 cyclosporin 488 cytochrome c 847 cytochrome c peroxidase 849 dihydrofolate reductase 807 DNA 214, 223,228,229, 241 DNA complex... 

A reaction that is ordinarily of minor consequence in the animal body but which may be enhanced by a deficiency of sulfite oxidase is the reductive coupling of two molecules of sulfite to form thiosulfate (Eq. 24-45, step e). Several organic hydrodisulfide derivatives such as thiocysteine, thioglutathione, and thiotaurine occur in animals in small amounts. Another biosynthetic pathway, outlined in Eq. 24-47 converts sulfite and PEP into coenzyme M (Fig. 15-22)475/475a This cofactor is needed not only for methane formation (Fig. 15-2) but also for utilization of alkenes by soil bacteria.4751 ... 

While sulfide is toxic to cytochrome (c) oxidase the most important enzyme of the respiratoiy chain, at concentrations in the tens of pM, thiosulfate is not Thus, the animal has produced a soluble and excretable detoxification product and protected animal respiration. This thiosulfate still contains large amounts of energy and can serve as a substrate for bacterial chemoautotrophic metabolism. The bacterial endosymbionts can utilize the thiosulfate along with sulfide to fix CO2 (5Q) and supply the host s nutritional needs. 

The cyanide antidote kit contains amyl nitrate, sodium nitrate, and sodium thiosulfate. Nitrates convert hemoglobin to methemoglobin, which in turn competes for cyanide with the mitochondrial oxidase complex. Amyl nitrate pearls, administered by inhalation, can be utilized as a first aid measure when intravenous (IV) access is impossible or will be delayed. If IV access is available, IV sodium nitrate is preferred, followed by sodium thiosulfate. Sodium thiosulfate reacts with cyanide to form nontoxic thiocyanate, which is then excreted into the urine. 

Sudden death in horses can be caused by consumption of cyanide-containing plants, such as sorghum. The cyanide ion forms a complex with cytochrome oxidase. This prevents electron transport and the utilization of oxygen by body tissues. As a consequence, the circulating blood is well oxygenated and is bright cherry red in color. This condition is an emergency, and treatment requires the prompt intravenous administration of both sodium thiosulfate and sodium nitrite. 

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