hyperoxaluria/glutathione

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Role of glutathione on renal mitochondrial status in hyperoxaluria.

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Role of glutathione on kidney mitochondrial integrity and function during stone forming process in hyperoxaluric state was investigated in male albino rats of Wistar strain. Hyperoxaluria was induced by feeding ethylene glycol (EG) in drinking water. Glutathione was depleted by administering

Protective effects of N-acetylcysteine against hyperoxaluria induced mitochondrial dysfunction in male wistar rats.

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The purpose of the present study was to evaluate the nephro-protective potential of N-acetylcysteine against hyperoxaluria-induced renal mitochondrial dysfunction in rats. Nine days dosing of 0.4 % ethylene glycol +1 % ammonium chloride, developed hyperoxaluria in male wistar rats which resulted in

Effect of cyclosporin on liver antioxidants and the protective role of vitamin E in hyperoxaluria in rats.

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This study aimed to evaluate whether administration of cyclosporin to hyperoxaluric rats affects liver antioxidant status, and whether pretreatment with vitamin E reverses the effect. Male Wistar rats were divided into two major groups of 40. One group was given vitamin E. Both major groups were

Renal oxidative vulnerability due to changes in mitochondrial-glutathione and energy homeostasis in a rat model of calcium oxalate urolithiasis.

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Calcium oxalate monohydrate (COM) crystals are the commonest component of kidney stones. Oxalate and COM crystals in renal cells are thought to contribute to pathology via prooxidant events. Using an in vivo rat model of crystalluria induced by hyperoxaluria plus hypercalciuria [ethylene glycol (EG)

Effects of angiotensin II subtype 1 receptor blockade by losartan on tubulointerstitial lesions caused by hyperoxaluria.

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OBJECTIVE Hyperoxaluria is a recognized cause of tubulointerstitial lesions and this circumstance could contribute to cause chronic renal disease. The renin-angiotensin system has a critical role in the development of interstitial fibrosis, mostly by angiotensin II type 1 receptor stimulation of

Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan.

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Oxalate/calcium oxalate toxicity is mediated through generation of reactive oxygen species in a process that partly depends upon events that induce mitochondrial damage. Mitochondrial dysfunction is an important event favoring stone formation. The objective of the present study was to investigate

Vitamin E therapy prevents hyperoxaluria-induced calcium oxalate crystal deposition in the kidney by improving renal tissue antioxidant status.

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OBJECTIVE To determine whether vitamin E prevents hyperoxaluria-induced stone formation, using a new animal model of calcium oxalate stone disease, as our previous in- vitro and in-vivo studies showed that oxalate and hyperoxaluria induce free-radical generation, which results in peroxidative injury

Modulatory effect of 4-phenyl butyric acid on hyperoxaluria-induced renal injury and inflammation.

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Hyperoxaluria-associated deposition of calcium oxalate crystals results from oxalate-induced renal injury and inflammation. The present study was designed to evaluate the effect of 4-Phenyl butyric acid (4-PBA), a chemical chaperone, in ethylene glycol-induced hyperoxaluria and compare its effect

Supplementation of vitamin E and selenium prevents hyperoxaluria in experimental urolithic rats.

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Renal injury is considered as one of the prerequisites for calcium oxalate retention. In order to determine the role of lipid peroxidation related effects for hyperoxaluria, we evaluated the alterations in lipid peroxidation, antioxidants and oxalate synthesizing enzymes in lithogenic rats with

1,2,3,4,6-Penta-O-galloyl-beta-D-glucose reduces renal crystallization and oxidative stress in a hyperoxaluric rat model.

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Adhesion of calcium oxalate (CaOx) crystals to kidney cells may be a key event in the pathogenesis of kidney stones associated with marked hyperoxaluria. Previously, we found that 1,2,3,4,6-penta-O-galloyl-β-D-glucose (PGG), isolated from a traditional medicinal herb, reduced CaOx crystal adhesion

Restoration of tissue antioxidants and prevention of renal stone deposition in vitamin B6 deficient rats fed with vitamin E or methionine.

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Observed loss in body weight gain, increased lipid peroxidation reaction, decreased concentrations of antioxidants, ascorbic acid, alpha-tocopherol and reduced glutathione and antioxidant enzymes, glutathione peroxidase and catalase and increased concentration of hydroperoxides and hydroxyl radicals

Oxalate mediated nephronal impairment and its inhibition by c-phycocyanin: a study on urolithic rats.

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The assumption of oxidative stress as a mechanism in oxalate induced renal damage suggests that antioxidants might play a beneficial role against oxalate toxicity. An in vivo model was used to investigate the effect of C-phycocyanin (from aquatic micro algae; Spirulina spp.), a known antioxidant,

Prophylaxis and therapeutic effects of raspberry (Rubus idaeus) on renal stone formation in Balb/c mice.

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OBJECTIVE To evaluate the prophylactic potential of herbal decoction from Rubus idaeus, a medicinal plant widely used in the Middle East to treat kidney stones, by assessing the effect of administration in experimentally induced calcium oxalate (CaOx) nephrolithiasis in mice. METHODS This study was

Cells of proximal and distal tubular origin respond differently to challenges of oxalate and calcium oxalate crystals.

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LLC-PK1 and Madin-Darby canine kidney (MDCK) cells were used to study the role of free radicals in renal epithelial injury during exposure to oxalate ions (Ox) and calcium oxalate monohydrate (COM) crystals. The cell cultures were exposed for 120 or 240 min to 1.0 mmol Ox or 1.0 mmol Ox plus 500

Rapid communication: protective effect of a nuclear factor kappaB inhibitor, pyrolidium dithiocarbamate, in the kidney of rats with nephrolithiasis induced by ethylene glycol.

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OBJECTIVE To study the protective effects of a selective nuclear factor kappa B (NF-kappaB) inhibitor, pyrolidium dithiocarbamate (PDTC), on ethylene glycol-induced crystal deposition in the renal tubules, renal toxicity, as well as inducible nitric oxide synthase (iNOS) and NF-kappaB activities in

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