Thiosulfate, urinary

In the case of life-threatening hydrogen sulfide poisoning, measurements of blood sulfide or urinary thiosulfate levels may be used to confirm exposure. However, samples need to be taken within two hours of exposure in order to be useful. The tests for measuring sulfide in the blood or thiosulfate in the urine are described in Section 2.7.1. 

Urinary thiosulfate levels were measured in volunteers exposed to 8, 18, or 30 ppm of hydrogen sulfide for 30-45 minutes and compared to levels in unexposed individuals at a pelt processing plant (Kangas... 

The usefulness of urinary thiosulfate as an indicator of nonfatal hydrogen sulfide toxicity has been studied (Kangas and Savolainen 1987). Urinary samples for thiosulfate were obtained from volunteers exposed by inhalation to 8, 18, or 30 ppm of hydrogen sulfide for 30-45 minutes (the occupational exposure limit of 10 ppm for 8 hours was never exceeded). Excretion of urinary thiosulfate increased linearly up to 15 hours postexposure. Beyond 15 hours, the urinary thiosulfate concentration remained low, possibly indicating that most of the absorbed hydrogen sulfide was metabolized or excreted within 15 hours. 

Urinary thiosulfate levels as an exposure biomarker have been examined in rabbits (Kage et al. 1992). Urinary thiosulfate levels were detected in rabbit urine 24 hours after exposure to nonfatal concentrations of 100-200 ppm of hydrogen sulfide. Thiosulfate levels could be detected in the blood for up to 2 hours following exposure, whereas blood sulfide was not detectable. Measurements of thiosulfate levels in the blood, lung, or brain were found following fatal exposures to 500-1,000 ppm of hydrogen sulfide in experimental animals. 

These effects are not specific for hydrogen sulfide, and further study is needed to correlate these effects with blood sulfide and urinary thiosulfate levels. 

After sulfide is oxidized to sulfate (the major metabolic pathway), sulfate is excreted in the urine (Beauchamp et al. 1984). A human volunteer exposed at a concentration of 18 ppm hydrogen sulfide for 30 min was found to have urinary thiosulfate concentrations of approximately 2, 4, 7, 30, and 5 /nnol/mM creatine 1, 2, 5, 15, and 17 h after exposure, respectively (Kangas and Savolainen 1987). Blood thiosulfate concentrations decreased in rabbits exposed to hydrogen sulfide at a concentration 100-200 ppm for 60 min from 0.061 /tmol/mL immediately after exposure to an undetectable amount after 4 h (Kage et al. 1992). Urine... 

Kangas, J., and H.Savolainen. 1987. Urinary thiosulfate as an indicator of exposure to hydrogen sulphide vapour. Clin. Chim. Acta 164(1) 7-10. 

Genetic deficiency of sulfite oxidase in humans develops in early infancy, with lethal outcome at the age of 2-3 years. The condition is associated with high urinary output of sulfite, thiosulfate and S-sulfo-L-cysteine, along with a marked decrease in urinary sulfate. The diseased... 

A nutritional molybdenum deficiency with clinical symptoms similar to those of sulfite oxidase deficiency was identified in a human patient receiving long-term total parenteral nutrition (TPN) (Abumurad et al. 1981). The clinical symptoms included irritability leading to coma, tachycardia, tachypnea, and night blindness. A reduced intake of protein and sulfur-amino acids alleviated the symptoms, but they were aggravated by infusion of sulfite. The biochemical findings were low tissue sulfite oxidase activity a 25-fold increase in thiosulfate excretion a 70% reduction in urinary output of sulfate and a marked rise in plasma methionine. The clinical symptoms of molybdenum deficiency were totally eliminated by daily supplementation of 300 pg of the element. 

Iereverre F, Mudd SH, Heizer WD and Faster L (1967) Sulfite oxidase deficiency studies of a patient with mental retardation, dislocated ocular lenses, and abnormal urinary excretion of S-sulfo-L-cys-teine, sulfite, and thiosulfate. Bioebem Med 1 187 -217. 

Organic sulfur metabolites are catabolized up to sulfate, which in turn is excreted via the urine. The final step of the pathway -the reduction of sulfite to sulfate - is dependent on the molybdenum-containing enzyme, sulfite oxidase. Both, a genetic disorder of sulfite oxidase synthesis or a molybdenum deficiency will reduce the urinary excretion of sulfate, but increase that of sulfite, S-sulfocysteine and thiosulfate. Due to the toxic effect of sulfite on the nervous system, this disease is characterized by mental retardation and dislocation of ocular lenses (Rajagopalan 1988). A marginal amount of molybdenum or sulfite oxidase worsen the sulfite detoxification of the... 

As with blood, urine analysis is used in clinical studies, and the relative concentrations of various ionic species are of great importance in both disease diagnostic and drug metabolism studies. For example, IC is used to determine urine oxalate concentrations. Urinary oxalate levels are an important parameter in urolithiasis research (kidney stones). Other anions that can be determined in urine using IC include phosphate, sulfate, bromide, citrate, nitrate, nitrite, and thiosulfate. As with blood and serum samples, both ultrafiltration and centrifugation are often used as sample cleanup steps. 

Sulfite oxidase (sulfite dehydrogenase) (EC 1.8.3.1). Urinary excretion of S-sulfo-L-cysteine, sulfite and thiosulfate, and virtual absence of urinary sulfate. Progressive neurological abnormalities, mental retardation, lens dislocatioiL Treatment with diet low in sulfur amino acids. Death in postnatal period possi-... 

It has been known for a long time that thiosulfate is present in normal human urine, but reliable methods for the determination of fairly low concentrations have not been available. A method based on the precipitation of the nickel-ethylenediamine complex of thiosulfate followed by iodometric determination was reported many years ago, but gives according to our experience unreliable results. We have earlier described a simple colorimetric method for determination of thiosulfate, based on the cyanolysis of thiosulfate to thiocyanate by the action of cyanide and cupric ions followed by determination of thiocyanate as its ferric ion complex. Unfortunately, this method is not sensitive enough for direct application to urine and, furthermore, other urinary compounds interfere in the cyanolysis reaction. It may, however, be used for assay of the very... 

J. H. Gast, K. Arai and F. Aldrich, Quantitative studies on urinary thiosulfate excretion by healthy hioman subjects,... 

These results show that urinary thiosulfate comes from the animal metabolism proper, and not, as had been believed for some time, from bacterial action in the digestive tract. It thus represents an intermediary... 

---