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Original Article Mechanism of 2-Deoxy-D-ribose-induced Damage in Pancreatic beta-cells.
Gwanpyo Koh, Jeong taek Woo, Dae Ho Lee, Seungjoon Oh, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Deok Bae Park
Diabetes & Metabolism Journal 2007;31(2):105-112
DOI: https://doi.org/10.4093/jkda.2007.31.2.105
Published online: March 1, 2007
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1Department of Internal Medicine, Cheju National University College of Medicine, Korea.
2Department of Medicine1, Cheju Nationa University College of Medicine, Korea.
3Department of Endocrinology & Metabolism, Kyung Hee University College of Medicine, Korea.

BACKGROUND
Mechanism for glucose toxicity is known to be an increased oxidative stress produced by multiple pathways. In our previous report, 2-deoxy-d-ribose (dRib) promoted apoptosis by increasing oxidative stress in a pancreatic beta-cell line. We performed this study to investigate the mechanism of dRib-induced damage of beta-cells. METHODS: HIT-T15 cells were cultured in RPMI-1640 medium with 40 mM dRib for 24 hours after pretreatment with various concentrations of a metal chelator (DTPA) and inhibitors of protein glycation (aminoguanidine and pyridoxamine). Cell viability was determined by MTT assay. Apoptosis was analyzed by flow cytometry with annexin V/PI double staining. RESULTS: DTPA, which inhibits the monosaccharide autoxidation, partially reversed dRib-induced cytotoxicity in a dose-dependent manner (P < 0.01). The cytotoxicity was also suppressed dose-dependently by aminoguanidine (AG) and pyridoxamine (PM) (P < 0.05 and P < 0.01, repectively). Flow cytometric analysis showed that pretreatment of DTPA and AG also reversed the dRib-triggered apoptosis in a dose-dependent manner. We assessed the additional protective effects of inhibitors of protein glycation from dRib-induced cytotoxiciy in the presence of a metal chelator. The additions of AG (P < 0.05) and PM (P < 0.01) significantly reduced the cytotoxicity compared with DTPA alone group. CONCLUSION: This results suggest that dRib produce cytotoxicity and apoptosis through the mechanisms of advanced glycation endproducts (AGEs) formation including the monsaccharide autoxidation and protein glycation in pancreatic beta-cell. Thus, dRib could be a surrogate for glucose in the study of glucose toxicity and chronic diabetic complications.

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    Mechanism of 2-Deoxy-D-ribose-induced Damage in Pancreatic beta-cells.
    Korean Diabetes J. 2007;31(2):105-112.   Published online March 1, 2007
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Koh G, Woo Jt, Lee DH, Oh S, Kim SW, Kim JW, Kim YS, Park DB. Mechanism of 2-Deoxy-D-ribose-induced Damage in Pancreatic beta-cells.. Diabetes Metab J. 2007;31(2):105-112.
DOI: https://doi.org/10.4093/jkda.2007.31.2.105.

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