Most Viewed Abstracts
1. Report Shows Shift in Starting Salaries for Physicians 2. 2008 Exclusive Survey—Earnings: Good news for primary care income 3. Medicare pay-for-reporting effort draws fire from frustrated doctors 4. Debunking Myths in the US Healthcare System 5. Doctors and the DEA Free full text
Your Article Summary
2-Deoxy-d-ribose induces cellular damage by increasing oxidative stress and protein glycation in a pancreatic beta-cell line
Metabolism-Clinical and Experimental, 10/13/09
Koh G et al. – On incubation with albumin, dRib increased dicarbonyl and advanced glycation end product formation. Aminoguanidine and pyridoxamine significantly decreased the dicarbonyl and advanced glycation end product augmentations. These results suggest that both oxidative stress and protein glycation are important mechanisms of dRib–induced damage in a pancreatic beta–cell line.
Related Articles
Kaempferol protects HIT-T15 pancreatic beta cells from 2-deoxy-D-ribose-induced oxidative damage
Phytotherapy Research, 10/20/09
Relevance Score: 80%
Today in Basic Science/Genetics...keeping you current
Receive free subspecialty "5-minute updates" via email
Immunological detection of fructose-derived advanced glycation end-products
Laboratory Investigation, 03/19/10
Involvement of Estrogen Receptor Variant ER-[alpha]36, Not GPR30, in Nongenomic Estrogen Signaling
Molecular Endocrinology, 03/19/10
The Transcription Factor ATF4 Promotes Skeletal Myofiber Atrophy during Fasting
Molecular Endocrinology, 03/19/10
Article Search
Sponsor


See Latest Articles


