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      Hyper-Vascular Change and Formation of Advanced Glycation Endproducts in the Peritoneum Caused by Methylglyoxal and the Effect of an Anti-Oxidant, Sodium Sulfite

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          Objective: Methylglyoxal (MGO) in a heat-sterilized conventional PD solution may damage peritoneal cells directly and/or indirectly by producing advanced glycation endproducts (AGEs). This study was conducted to (a) examine the acute effect of MGO on the peritoneum (including AGE formation) and (b) study the possible AGE suppressive effect of an anti-oxidant, sodium sulfite. Method: (1) Human serum albumin (HAS) was continuously incubated with MGO (50 m M) at 37°C for as long as 14 days and the fluorescence intensity (FI) was determined (em. 440, ex. 370). (2) Three types of test solutions – (i) saline; (ii) MGO (20 m M), and (iii) MGO with sodium sulfite (30 m M) – were administered intraperitoneally to 8-week-old rats once a day for 5 consecutive days. The parietal peritoneum was examined macroscopically on the 6th day for immunostaining of anti-AGE antibodies. Result: (1) An increase in FI of HSA was observed as a function of the incubation period in the MGO solution. (2) Prominent hypervascularity and intense immunostaining of anti-AGE Ab were noted in MGO-treated rats, whereas the macroscopic alterations were suppressed in the rats that had been treated with sodium sulfite. Conclusion: MGO-induced hypervascularity and AGE formation in the peritoneum, as well as macroscopic alterations were suppressed by sodium sulfite. This may indicate that there is a risk of MGO causing a peritoneal injury and that the therapeutic potential of an anti-oxidant for this type of injury may exist.

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          Glucose degradation product methylglyoxal enhances the production of vascular endothelial growth factor in peritoneal cells: role in the functional and morphological alterations of peritoneal membranes in peritoneal dialysis.

          Peritoneal membrane permeability deteriorates in peritoneal dialysis (PD) patients. We test whether glucose degradation products (GDPs) in PD fluids, glyoxal, methylglyoxal and 3-deoxyglucosone, stimulate the production of vascular endothelial growth factor (VEGF), a factor known to enhance vascular permeability and angiogenesis. VEGF increased in cultured rat mesothelial and human endothelial cells exposed to methylglyoxal, but not to glyoxal or 3-deoxyglucosone. VEGF also increased in peritoneal tissue of rats given intraperitoneally methylglyoxal. VEGF and carboxymethyllysine (CML) (formed from GDPs) co-localized immunohistochemically in mesothelial layer and vascular walls of the peritoneal membrane of patients given chronic PD. By contrast, in the peritoneum of non-uremic subjects, VEGF was identified only in vascular walls, in the absence of CML. VEGF production induced by GDPs may play a role in the progressive deterioration of the peritoneal membrane.
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            Induction of synthesis and secretion of interleukin 1 beta in the human monocytic THP-1 cells by human serum albumins modified with methylglyoxal and advanced glycation endproducts.

            Human serum albumin modified with 1-2 methylglyoxal residues per molecule of protein (MGmin-HSA) stimulated the synthesis and secretion of interleukin 1 beta (IL-1 beta) from human monocytic THP-1 cells in vitro. It was a more potent inducer of IL-1 beta synthesis than human serum albumin highly-modified with glucose-derived advanced glycation endproducts (AGE-HSA). With 20 microM ligand. IL-1 beta synthesis was (pg/10(6) cells): MGmin-HSA 484.5 +/- 50.3; AGE-HSA 30.6 +/- 2.0 (n = 3). IL-1 beta synthesis increased markedly with MGmin-HSA concentrations > 5 microM. IL-1 beta synthesis and secretion from monocytes in response to methylglyoxal-modified proteins in vivo may contribute to the development of macro- and micro-angiopathy, particularly in diabetes mellitus.

              Author and article information

              Am J Nephrol
              American Journal of Nephrology
              S. Karger AG
              December 2003
              21 November 2003
              : 23
              : 6
              : 390-394
              aDivision of Kidney and Hypertension, Tokyo Jikei University School of Medicine, Tokyo, and bJapan Science and Technology Corporation, Tokyo, Japan
              74065 Am J Nephrol 2003;23:390–394
              © 2003 S. Karger AG, Basel

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              Page count
              Figures: 5, References: 17, Pages: 5
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/74065
              Original Report: Laboratory Investigation


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