Thiosulfate in the form of sodium thiosulfate (STS) is a major oxidation product of hydrogen sulfide (H₂S), an endogenous signaling molecule and the third member of the gasotransmitter family. STS is currently used in the clinical treatment of acute cyanide poisoning, cisplatin toxicities in cancer therapy, and calciphylaxis in dialysis patients. Burgeoning evidence show that STS has antioxidant and anti-inflammatory properties, making it a potential therapeutic candidate molecule that can target multiple molecular pathways in various diseases and drug-induced toxicities. This review discusses the biochemical and molecular pathways in the generation of STS from H₂S, its clinical usefulness, and potential clinical applications, as well as the molecular mechanisms underlying these clinical applications and a future perspective in kidney transplantation.

Hibernation consists of periods of low metabolism, called torpor, interspersed by euthermic arousal periods. During deep and daily (shallow) torpor, the number of circulating leukocytes decreases, although circulating cells, is restored to normal numbers upon arousal. Here, we show that neutropenia, during torpor, is solely a result of lowering of body temperature, as a reduction of circulating also occurred following forced hypothermia in summer euthermic hamsters and rats that do not hibernate. Splenectomy had no effect on reduction in circulating neutrophils during torpor. Margination of neutrophils to vessel walls appears to be the mechanism responsible for reduced numbers of neutrophils in hypothermic animals, as the effect is inhibited by pretreatment with dexamethasone. In conclusion, low body temperature in species that naturally use torpor or in nonhibernating species under forced hypothermia leads to a decrease of circulating neutrophils as a result of margination. These findings may be of clinical relevance, as they could explain, at in least part, the benefits and drawbacks of therapeutic hypothermia as used in trauma patients and during major surgery.