Skip Navigation
Skip to contents

Diabetes Metab J : Diabetes & Metabolism Journal

Search
OPEN ACCESS

Search

Page Path
HOME > Search
1 "Autoxidation"
Filter
Filter
Article category
Keywords
Publication year
Authors
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
Korean Diabetes J. 2007;31(2):105-112.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.105
  • 2,226 View
  • 21 Download
  • 2 Crossref
AbstractAbstract PDF
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.

Citations

Citations to this article as recorded by  
  • Isolation of Citrus Peel Flavonoid Bioconversion Microorganism and Inhibitory Effect on the Oxidative Damage in Pancreatic Beta Cells
    Chi-Deok Park, Hee-Kyung Jung, Chang-Ho Park, Yoo-Seok Jung, Joo-Heon Hong, Hee-Sun Ko, Dong-Hee Kang, Hyun-Soo Kim
    KSBB Journal.2012; 27(1): 67.     CrossRef
  • Kaempferol protects HIT‐T15 pancreatic beta cells from 2‐deoxy‐D‐ribose‐induced oxidative damage
    Yun Jung Lee, Kwang Sik Suh, Moon Chan Choi, Suk Chon, Seungjoon Oh, Jeong‐Taek Woo, Sung‐Woon Kim, Jin‐Woo Kim, Young Seol Kim
    Phytotherapy Research.2010; 24(3): 419.     CrossRef

Diabetes Metab J : Diabetes & Metabolism Journal
Close layer