Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 microg/ml of COM crystals averaging 1.0 microm in size. Exposure of both LLC-PK1 and MDCK cells to Ox alone increased the leakage of lactate dehydrogenase, which was further enhanced when cells were exposed to Ox + COM crystals. The release of lactate dehydrogenase from the LLC-PK1 cell line, however, was significantly higher than that from MDCK cells. LLC-PK1 cells also showed a significant increase in malondialdehyde (MDA) content on Ox challenge. MDA content was even higher when LLC-PK1 cells were challenged with Ox + COM crystals. However, in MDCK cells, the elevated MDA content was similar in both treatment groups, suggesting that these cells may be more resistant to the calcium oxalate crystals. Glutathione peroxidase activity was decreased in both LLC-PK1 and MDCK cells. Challenging cells with Ox + COM resulted in decreased catalase activity in LLC-PK1, but increased catalase activity in MDCK cells. Superoxide dismutase activity and reduced glutathione content were not significantly different in either cell type when challenged with Ox or Ox + COM. Previous in vivo animal studies yielded indirect evidence for the increased lipid peroxidation during hyperoxaluria-induced nephrolithiasis. However, in an animal model, it is difficult to separate the effect of Ox from Ox in combination with COM crystals. This study suggests that the injury to renal tubular epithelial cells is accompanied by lipid peroxidation when exposed to Ox. The injury is augmented when COM crystals are included. LLC-PK1 cells are more susceptible to Ox-associated injury than MDCK cells.
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PMID:Cells of proximal and distal tubular origin respond differently to challenges of oxalate and calcium oxalate crystals. 1054 Dec 82

This study amied to investigate the effects of Orthosiphon grandiflorum on the renal tubular cell injury induced by oxalate and the inhibitory effects of O. grandiflorum on urinary deposit formation in an animal model and compared the results with those from a potassium citrate treatment. Rats were divided into three groups: an untreated stone-forming group, an O. grandiflorum-treated stone-forming group and a potassium citrate-treated stone forming group. Ethylene glycol (0.5%) was administered to the rats during the last week, and vitamin D3 (0.5 mum) was force fed to induce hyperoxaluria and kidney calcium oxalate crystal deposition. Twenty-four hour urine samples were collected before and after inducing crystal deposits. Rats were killed and both kidneys were harvested after 3 weeks. Bisected kidneys were examined under a polarized light microscope to determine the number of crystals. The renal tissue superoxide dismutase and catalase levels were measured by Western blot. Oxidative stress was examined by 8-OHdG immunohistofluorescence. O. grandiflorum and potassium citrate have the ability to alkalinize urine. Among all groups, the number of crystal deposits and the level of 8-OHdG staining decreased significantly in the O. grandiflorum-treated stone forming group, as compared to the other groups. Superoxide dismutase and catalase levels also increased significantly in the O. grandiflorum-treated stone-forming group, as compared with the untreated stone-forming group. The results indicate that O. grandiflorum has a significant inhibitory effect on crystal deposition in the calcium oxalate-stone-forming rat model.
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PMID:Orthosiphon grandiflorum has a protective effect in a calcium oxalate stone forming rat model. 2022 91

Quercetin and hyperoside (QH) are the two main constituents of the total flavone glycosides of Flos Abelmoschus manihot, which has been prescribed for treating chronic kidney disease for decades. This study aimed to investigate the effect of QH on calcium oxalate (CaOx) formation in ethylene glycol (EG)-fed rats. Rats were divided into three groups: an untreated stone-forming group, a QH-treated stone-forming group (20 mg/kg/day) and a potassium citrate-treated stone-forming group (potassium citrate was a worldwide-recognized calculi-prophylactic medicine). Ethylene glycol (0.5 %) was administered to the rats during the last week, and vitamin D3 was force-fed to induce hyperoxaluria and kidney calcium oxalate crystal deposition. 24 h urine samples were collected before and after inducing crystal deposits. Rats were killed and both kidneys were harvested after 3 weeks. Bisected kidneys were examined under a polarized light microscope for semi-quantification of the crystal-formation. The renal tissue superoxide dismutase and catalase levels were measured by Western blot. QH and potassium citrate have the ability to alkalinize urine. The number of crystal deposits decreased significantly in the QH-treated stone-forming group as compared to the other groups. Superoxide dismutase and catalase levels also increased significantly in the QH-treated stone-forming group, as compared with the untreated stone-forming group. QH administration has an inhibitory effect on the deposition of CaOx crystal in EG-fed rats and may be effective for preventing stone-forming disease.
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PMID:Prophylactic effects of quercetin and hyperoside in a calcium oxalate stone forming rat model. 2508 99