ArticleIndian journal of pharmacology
Renal mitochondria can withstand hypoxic/ischemic injury secondary to renal failure in uremic rats pretreated with sodium thiosulfate.
Article in Indian journal of pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Advances in the clinical applications of sodium thiosulphate.Annals of medicine · 2026Review
- MOTS-c preserves mitochondrial subpopulation bioenergetics and genome integrity to attenuate cardiac ischemia reperfusion injury.Molecular biology reports · 2026Article
- Antihypertensive Effects of a Sodium Thiosulfate-Loaded Nanoparticle in a Juvenile Chronic Kidney Disease Rat Model.Antioxidants (Basel, Switzerland) · 2024Article
- Evaluation of prophylactic efficacy of sodium thiosulfate in combating I/R injury in rat brain: exploring its efficiency further in vascular calcified brain slice model.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Review
- HBiomolecules · 2022Review
- Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases.Biomolecules · 2021Review
- Hydrogen Sulfide Metabolite, Sodium Thiosulfate: Clinical Applications and Underlying Molecular Mechanisms.International journal of molecular sciences · 2021Review
- PINK1/Parkin-mediated mitophagy is activated in cisplatin nephrotoxicity to protect against kidney injury.Cell death & disease · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSodium thiosulfate (STS) is a potent drug used to treat calcific uremic arteriopathy in dialysis patients and its mode of action is envisaged by calcium chelation and antioxidant potential. STS's action on mitochondrial dysfunction, one of the major players in the pathology of vascular calcification is yet to be explored.
methodsAdenine (0.75%, 28 days)-treated vascular calcified rat kidney was used to isolate mitochondria, where the animal was administered with or without STS for 28 days. Isolated mitochondria were subjected to physiological oxidative stress by nitrogen gas purging (hypoxia/ischemia-reperfusion injury) to assess mitochondrial recovery extent due to STS treatment in vascular calcified rat kidney.
resultsThe results confirmed an elevated oxidative stress and deteriorated mitochondrial enzyme activities in all groups except the drug-treated group.
conclusionThe STS treatment, besides rendering renal protection against adenine-induced renal failure, also helped to maintain mitochondrial functional integrity in a later insult due to hypoxia/ischemia-reperfusion injury.
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