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DOI 10.1002/mnfr.200400111

Медицинская библиотека · Molecular nutrition & food research · 2005

Fate of the glucose degradation products 3-deoxyglucosone and glyoxal during peritoneal dialysis.

Tauer Andreas, Bender Thorsten O, Fleischmann Erwin H, Niwa Toshimitsu, Jörres Achim, Pischetsrieder Monika

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Conventional fluids for peritoneal dialysis (PD) contain reactive glucose degradation products (GDPs) as a result of glucose breakdown during heat-sterilization. GDPs in PD fluids (PDFs) have been associated with the progressive alteration of the peritoneal membrane during long-term PD by cytotoxic effects and formation of advanced glycation endproducts (AGEs). In this study, we investigated the possible fate of two characteristic GDPs, 3-deoxyglucosone (3-DG) and glyoxal, during PD. In vivo, 3-DG and glyoxal concentrations, which were analyzed by high-performance liquid chromatography (HPLC), decreased in PDFs by 78% and 88% during 4 h of dwell time. The PDFs were then incubated in vitro in the presence of the most important reaction partners of GDPs in the peritoneal cavity. Neither human peritoneal mesothelial cells, human peritoneal fibroblasts, soluble protein, an insoluble collagen surface, nor components of spent dialysate led to a significant reduction of 3-DG or glyoxal after 6 h. Only after long-term incubation, a noticeable decrease of 3-DG was observed (-37% after three weeks), more likely due to spontaneous degradation reaction than formation of advanced glycation endproducts. These results suggest that in the course of PD, 3-DG, and glyoxal are absorbed into the organism and thus might contribute to the systemic pool of reactive carbonyl compounds.

Для цитирования: Tauer Andreas, Bender Thorsten O, Fleischmann Erwin H, Niwa Toshimitsu, Jörres Achim, Pischetsrieder Monika. Fate of the glucose degradation products 3-deoxyglucosone and glyoxal during peritoneal dialysis.. Molecular nutrition & food research. 2005. DOI: 10.1002/mnfr.200400111.

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