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Effects of d-ribose on human erythrocytes: Non-enzymatic glycation of hemoglobin, eryptosis, oxidative stress and energy metabolism
d-Ribose is not only an important component of some biomacromolecules, but also an active pentose with strong reducibility and non-enzymatic glycation ability. Previous studies reported the diverse role of d-ribose in different cells. In this study, the effects of d-ribose on non-enzymatic glycation...
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Published in: | Blood cells, molecules, & diseases molecules, & diseases, 2023-03, Vol.99, p.102725-102725, Article 102725 |
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Main Authors: | , , , , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | d-Ribose is not only an important component of some biomacromolecules, but also an active pentose with strong reducibility and non-enzymatic glycation ability. Previous studies reported the diverse role of d-ribose in different cells. In this study, the effects of d-ribose on non-enzymatic glycation of hemoglobin (Hb), as well as eryptosis, oxidative stress and energy metabolism of erythrocytes were observed by molecular fluorescence spectrophotometry, multi-wavelength spectrophotometry, high-pressure liquid chromatography (HPLC), mass spectrometry (MS) and flow cytometer. The results showed that d-ribose had the strongest non-enzymatic glycation ability to Hb in vitro when compared with other monosaccharides, and could enter the erythrocytes in a concentration-dependent manner, which was not inhibited by the specific glucose transporter 1 (GLUT1) inhibitor WZB117. In addition, d-ribose incubation increased the HbA1c, hemolysis, eryptosis, and ROS level of erythrocytes significantly more than that of d-glucose, however, no changes were observed in the levels of ATP, NADPH, and other intermediate energy metabolites in d-ribose treatment. Therefore, the strong non-enzymatic glycation ability of d-ribose may play an important role in erythrocyte damage. |
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ISSN: | 1079-9796 1096-0961 |
DOI: | 10.1016/j.bcmd.2023.102725 |