Indian journal of pharmacology · 2017
Renal mitochondria can withstand hypoxic/ischemic injury secondary to renal failure in uremic rats pretreated with sodium thiosulfate.
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Mohan Dhivya, Balasubramanian Eswari Dhivya, Ravindran Sriram, Kurian Gino A
Аннотация
BACKGROUND: Sodium 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.
METHODS: Adenine (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.
RESULTS: The results confirmed an elevated oxidative stress and deteriorated mitochondrial enzyme activities in all groups except the drug-treated group.
CONCLUSION: The 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.
METHODS: Adenine (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.
RESULTS: The results confirmed an elevated oxidative stress and deteriorated mitochondrial enzyme activities in all groups except the drug-treated group.
CONCLUSION: The 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.