Effect of calcium oxalate on renal cells as revealed by real-time measurement of extracellular oxidative burst

Gáspár, Szilveszter; Niculite, Cristina Mariana; Cucu, Dana; I, Marcu

doi:10.1016/j.bios.2009.12.013

Cited by 22 publications

(6 citation statements)

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“…Oxalate and calcium oxalate crystals cause the generation of superoxide radicals [ 29 ] mainly via PKC-regulated NADPH oxidase [ 30 , 31 ] and xanthine oxidase (XO) [ 32 ] [ 33 ] pathways in the mitochondria [ 34 ]. Free radical oxidants are short lived and their dismutation to H 2 O 2 , which represents the major oxidant burden, occurs at a very rapid rate [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Sodium Thiosulfate Ameliorates Oxidative Stress and Preserves Renal Function in Hyperoxaluric Rats

et al. 2015

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BackgroundHyperoxaluria 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.MethodsHyperoxaluria 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.ResultsChronic 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.ConclusionsSTS 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.

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Section: Discussionmentioning

confidence: 99%

Sodium Thiosulfate Ameliorates Oxidative Stress and Preserves Renal Function in Hyperoxaluric Rats

et al. 2015

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“…22 Mitochondria 4,23 and NADPH oxidase 11,19,24 are involved in ROS production. Ox or crystal induced cellular responses can be inhibited by antioxidants as well as by NADPH oxidase inhibitors.…”

Section: Tissue Culturementioning

confidence: 99%

Reactive Oxygen Species as the Molecular Modulators of Calcium Oxalate Kidney Stone Formation: Evidence from Clinical and Experimental Investigations

2013

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Purpose Idiopathic calcium oxalate kidney stones form while attached to Randall plaques, the subepithelial deposits on renal papillary surfaces. Plaque formation and growth mechanisms are poorly understood. Plaque formation elsewhere in the body is triggered by reactive oxygen species and oxidative stress. This review explores possible reactive oxygen species involvement in plaque formation and calcium oxalate nephrolithiasis. Materials and Methods A search of various databases for the last 8 years identified literature on reactive oxygen species involvement in calcium oxalate nephrolithiasis. The literature was reviewed and results are discussed. Results Under normal conditions reactive oxygen species production is controlled, increasing as needed and regulating crystallization modulator production. Reactive oxygen species overproduction or decreased antioxidants lead to oxidative stress, inflammation and injury, and are involved in stone comorbidity. All major chronic inflammation markers are detectable in stone patient urine. Patients also have increased urinary excretion of the IαI and the thrombin protein families. Results of a recent study of 17,695 participants in NHANES III (National Health and Nutrition Examination Survey) showed significantly lower antioxidants, carotene and β-cryptoxanthin in those with a kidney stone history. Animal model and tissue culture studies revealed that high oxalate, calcium oxalate and calcium phosphate crystals provoked renal cell reactive oxygen species mediated inflammatory responses. Calcium oxalate crystals induce renin up-regulation and angiotensin II generation. Nonphagocytic NADPH oxidase leads to reactive oxygen species production mediated by protein kinase C. The P-38 MAPK/JNK transduction pathway is turned on. Transcriptional and growth factors, and generated secondary mediators become involved. Chemoattractant and osteopontin production is increased and macrophages infiltrate the renal interstitium around the crystal. Phagocytic NADPH oxidase is probably activated, producing additional reactive oxygen species. Localized inflammation, extracellular matrix and fibrosis develop. Crystallization modulators have a significant role in inflammation and tissue repair. Conclusions Based on available data, Randall plaque formation is similar to extracellular matrix mineralization at many body sites. Renal interstitial collagen becomes mineralized, assisting plaque growth through the interstitium until the mineralizing front reaches papillary surface epithelium. Plaque exposure to pelvic urine may also be a result of reactive oxygen species triggered epithelial sloughing.

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“…A reduction in renal epithelial injury and CaOx crystal deposition was also seen in hyperoxaluric rats treated with atorvastatin [19]. Renal cells exposed to CaOx crystals secrete superoxide in real time as measured by an electrochemical superoxide biosensor [20]. The presence of antioxidants produced a significant reduction in cell injury and improved the antioxidant status of the cells when exposed to oxalate or CaOx or CaP crystals [2].…”

Section: Discussionmentioning

confidence: 95%

Temporal changes in the expression of mRNA of NADPH oxidase subunits in renal epithelial cells exposed to oxalate or calcium oxalate crystals

Khan

Byer

2010

Nephrology Dialysis Transplantation

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Effect of calcium oxalate on renal cells as revealed by real-time measurement of extracellular oxidative burst

Cited by 22 publications

References 44 publications

Sodium Thiosulfate Ameliorates Oxidative Stress and Preserves Renal Function in Hyperoxaluric Rats

Sodium Thiosulfate Ameliorates Oxidative Stress and Preserves Renal Function in Hyperoxaluric Rats

Reactive Oxygen Species as the Molecular Modulators of Calcium Oxalate Kidney Stone Formation: Evidence from Clinical and Experimental Investigations

Temporal changes in the expression of mRNA of NADPH oxidase subunits in renal epithelial cells exposed to oxalate or calcium oxalate crystals

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