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balkan nephropathy/glutation

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ČlanciKlinička ispitivanjaPatenti
Stranica 1 iz 23 rezultatima

Glutathione S-transferases T1 null genotype is associated with susceptibility to aristolochic acid nephropathy.

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OBJECTIVE This study aims to determine whether six polymorphisms of the genes involved in drug metabolism are associated with susceptibility to the development and progression of aristolochic acid nephropathy (AAN). METHODS In the study, 91 aristolochic acid nephropathy (AAN) cases and 152 healthy

Balkan endemic nephropathy and genetic variants of glutathione S-transferases.

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BACKGROUND Balkan endemic nephropathy (BEN) is a non-inflammatory, chronic, slow progressing kidney disease, frequently associated with urinary tract tumors. BEN displays familial clustering without an apparent Mendelian inheritance pattern. It has been suggested that environmental toxicants damage
In a previous paper a markedly decreased activity of delta-aminolevulinate dehydratase (ALA-D) in patients with endemic nephropathy and in 24.6% of their healthy family members, was found. In this study the possible mechanisms of the decreased enzyme activity and the level of erythrocyte glutathione

Selenium-dependent and selenium-non-dependent glutathione peroxidase in patients with Balkan endemic nephropathy.

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We studied the activity of erythrocyte selenium (Se)-dependent, Se-non-dependent glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in uremic patients (UP) in clinically healthy members from families affected with Balkan nephropathy (HMF/BEN) and in healthy volunteers from endemic
There is accumulating evidence that Balkan endemic nephropathy (BEN) is an environmental disease caused by aristolochic acids (AAs) released from the decomposition of Aristolochia clematitis L., an AA-containing weed that grows abundantly in the Balkan Peninsula. AA exposure has also been associated
Background: Experimental data show that superoxide dismutase 2 (SOD2) is involved in ochratoxin (OTA)-induced nephrotoxicity, whereas clinical data indicate the role of SOD2 rs4880 or glutathione peroxidase 1 (GPX1) rs1050450 polymorphisms in end-stage renal disease and
Although recent data suggest aristolochic acid as a putative cause of Balkan endemic nephropathy (BEN), evidence also exists in favor of ochratoxin A (OTA) exposure as risk factor for the disease. The potential role of xenobiotic metabolizing enzymes, such as the glutathione transferases (GSTs), in

Erythrocyte delta-aminolevulinate dehydratase measurements in Balkan endemic nephropathy.

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Balkan endemic nephropathy (BEN) is a chronic progressive kidney disease leading to renal insufficiency. The possible etiological role of some toxic factors was considered in this study by investigating the activity of erythrocyte delta-aminolevulinate dehydratase (ALA-D), an enzyme influenced by

Identification of NQO1 and GSTs genotype frequencies in Bulgarian patients with Balkan endemic nephropathy.

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BACKGROUND Polymorphisms in NAD[P]H:quinone oxidoreductase (NQO1) and glutathione S-transferases (GSTs) have been reported to be associated with an increased risk for environmentally and/or occupationally induced renal and bladder cancers. Genetic factors related to chronic nephropathy and to
Ochratoxin A (OTA), a nephrotoxic mycotoxin probably implicated in human Balkan endemic nephropathy and associated urothelial tumors, induces renal carcinomas in rodents and nephrotoxicity in pigs. OTA induces DNA-adduct formation, but the structure of the adducts and their role in nephrotoxicity
Balkan endemic nephropathy (BEN) is a chronic familial form of interstitial nephritis that might eventually lead to end stage renal disease. This nephropathy affects individuals living along of the Danube River and its tributaries in Serbia, Bosnia, Croatia, Bulgaria and Romania. The increased

Biomarkers of oxidative damage and antioxidant enzyme activities in pre-dialysis Balkan endemic nephropathy patients.

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OBJECTIVE To obtain more insight into molecular mechanisms underlying oxidative stress in Balkan endemic nephropathy (BEN), biomarkers of oxidative stress and antioxidant enzyme activities were studied in 38 pre-dialysis BEN patients, 21 healthy BEN family members and 36 healthy subjects from

Early proximal tubule injury in experimental aristolochic acid nephropathy: functional and histological studies.

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BACKGROUND Aristolochic acid (AA), the plant extract of Aristolochia species, is involved in the onset of progressive tubulointerstitial renal fibrosis in humans. Clinical and in vitro findings have previously suggested that the proximal tubule was the target of AA. METHODS Using a rat model of AA

How aspartame prevents the toxicity of ochratoxin A.

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The ubiquitous mycotoxin ochratoxin A (OTA) is found as a frequent contaminant of a large variety of food and feed and beverage such as beer, coffee and win. It is produced as a secondary metabolite of moulds from Aspergillus and Penicillium genera. Ochratoxin A has been shown experimentally to

Further arguments in favour of direct covalent binding of Ochratoxin A (OTA) after metabolic biotransformation.

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Ochratoxin A (OTA) is nephrotoxic to all animal species, carcinogenic for rats and mice and probably implicated in human Balkan endemic nephropathy and the associated urothelial tract tumour. Controversial results concerning genotoxicity and biotransformation of OTA have been generated. By (32)P
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