Abstract:
:Ascorbate is a reducing agent, which is also known to oxidize cellular components. Our proposed mechanism of the oxidative action is as follows: Ascorbate is concentrated in the pancreas and is leaked in adverse conditions, and oxidized to dehydroascorbate. The dehydroascorbate is carried into cells by a glucose transporter (GLUT) and reduced back to ascorbate. The reduction processes take electrons from other cellular components. Ascorbate or dehydroascorbate treatment elevated thiobarbituric acid-reactive substance (TBARS) concentrations in pancreas. The elevations in TBARS concentrations were blocked by cytochalasin B, a GLUT inhibitor. To confirm further the prooxidative action, changes in glutathione content were quantified. Glutathione concentrations were lower in ascorbate- or dehydroascorbate-treated groups. The ascorbate-induced decrease in glutathione was blocked by cytochalasin B. To prevent oxidation of ascorbate to dehydroascorbate, glutathione was added to the medium. The ascorbate plus glutathione and dehydroascorbate plus glutathione groups showed lower TBARS concentrations than those of the ascorbate and dehydroascorbate groups, respectively. There were changes in the morphology of Langerhans islets following ascorbate treatment, which disappeared following treatment with ascorbate plus cyto-chalasin B. The observations indicate that ascorbate generates oxidative stress and affects the structure of islets.
journal_name
Endocrinejournal_title
Endocrineauthors
Brown S,Georgatos M,Reifel C,Song JH,Shin SH,Hong Mdoi
10.1385/ENDO:18:1:91subject
Has Abstractpub_date
2002-06-01 00:00:00pages
91-6issue
1eissn
1355-008Xissn
1559-0100pii
ENDO:18:1:91journal_volume
18pub_type
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