Sodium thiosulfate ameliorates oxidative stress and preserves renal function in hyperoxaluric ratsBijarnia, R. K., Bachtler, M., Chandak, P. G., van Goor, H. & Pasch, A., 30-Apr-2015, In : PLoS ONE. 10, 4, 16 p., e0124881.
Research output: Contribution to journal › Article › Academic › peer-review
BACKGROUND: Hyperoxaluria causes crystal deposition in the kidney, which leads to oxidative stress and to injury and damage of the renal epithelium. Sodium thiosulfate (STS, Na2S2O3) is an anti-oxidant, which has been used in human medicine for decades. The effect of STS on hyperoxaluria-induced renal damage is not known.
METHODS: Hyperoxaluria and renal injury were induced in healthy male Wistar rats by chronic exposure to ethylene glycol (EG, 0.75%) in the drinking water for 4 weeks. The treatment effects of STS, NaCl or Na2SO4 were compared. Furthermore, the effects of STS on oxalate-induced oxidative stress were investigated in vitro in renal LLC-PK1 cells.
RESULTS: Chronic EG exposure led to hyperoxaluria, oxidative stress, calcium oxalate crystalluria and crystal deposition in the kidneys. Whereas all tested compounds significantly reduced crystal load, only STS-treatment maintained tissue superoxide dismutase activity and urine 8-isoprostaglandin levels in vivo and preserved renal function. In in vitro studies, STS showed the ability to scavenge oxalate-induced ROS accumulation dose dependently, reduced cell-released hydrogen peroxide and preserved superoxide dismutase activity. As a mechanism explaining this finding, STS was able to directly inactivate hydrogen peroxide in cell-free experiments.
CONCLUSIONS: STS is an antioxidant, which preserves renal function in a chronic EG rat model. Its therapeutic use in oxidative-stress induced renal-failure should be considered.
|Number of pages||16|
|Publication status||Published - 30-Apr-2015|
- OXALATE CRYSTAL DEPOSITION, CALCIUM-OXALATE, VASCULAR CALCIFICATION, HEMODIALYSIS-PATIENTS, STONE FORMATION, CELL INJURY, VITAMIN-E, KIDNEY, CALCIPHYLAXIS, DISEASE