ABSTRACT
Recent advances in endoscopic imaging of the esophagus have revolutionized the diagnostic capability for detecting premalignant changes and early esophageal malignancy. In this article, we review the practical application of narrow-band imaging focusing on diseases of the esophagus, including Barrett’s esophagus, adenocarcinoma, and squamous cell carcinoma.
ABSTRACT
Recent advances in endoscopic imaging of the esophagus have revolutionized the diagnostic capability for detecting premalignant changes and early esophageal malignancy. In this article, we review the practical application of narrow-band imaging focusing on diseases of the esophagus, including Barrett’s esophagus, adenocarcinoma, and squamous cell carcinoma.
ABSTRACT
The observation that ascorbate known to retain pro-oxidant properties induces cell death in a number of immortal cell lines, led us to examine its mechanism and whether it is involved in oxidative stress injury in such asocorbate-enriched tissue cells as hepatocytes. In rat liver homogenates, higher concentrations (1 and 3 mM) of ascorbate suppressed lipid peroxide productions but lower concentrations (0.1 and 0.3 mM) did not. In contrast to the homogenate, ascorbate increased lipid peroxide production in liver slices in a concentration dependant manner. Iso-ascorbate, the epimer of ascorbate did not cause an increase the oxidative stress in liver slices. This differential effect between homogenates and liver slices implies that cellular integrity is required for ascorbate to induce oxidative stress. Wortmannin, an inhibitor of the GLUT (glucose transporter) thought to transport dehydroascorbate into cells, inhibited [14C]- ascorbate uptake and suppressed oxidative stress in liver slices. Wortmannin suppressed that [14C]- ascorbate uptake by GLUT following oxidation to [14C]dehydroascorbate. Taken together, these observations support our hypothesis that ascorbate is oxidized to dehydroascorbate by molecular oxygen in solution (i.e., plasma and culture medium) which is then carried into hepatocytes (via a GLUT) where it is reduced back to ascorbate causing oxidative stress.
Subject(s)
Animals , Male , Rats , Androstadienes/pharmacology , Ascorbic Acid/metabolism , Biological Transport , Edetic Acid/pharmacology , Glutathione/metabolism , In Vitro Techniques , Liver/drug effects , Oxidation-Reduction/drug effects , Oxidative Stress/drug effects , Rats, Sprague-Dawley , Thiobarbituric Acid Reactive Substances/metabolism , Time FactorsABSTRACT
Pro-oxidant properties of ascorbate have been studied with uses of brain tissues and neuronal cells. Here we address potential mechanism of ascorbate coupling with glutamate to generate oxidative stress, and the role which oxidized ascorbate (dehydroascorbate) transport plays in oxidative neuronal injury. Ascorbate in neurones can be depleted by adding glutamate in culture medium since endogenous ascorbate can be exchanged with glutamate, which enhances ascorbate/ dehydroascorbate transport by depleting ascorbate in the neurons with the glutamate-heteroexchange. However, ascorbate is known readily being oxidized to dehydroascorbate in the medium. Glutamate enhanced the dehydroascorbate uptake by cells via a glucose transporter (GLUT) from extracellular region, and cytosolic dehydroascorbate enhanced lipid peroxide production and reduced glutathione (GSH) concentrations. Iso-ascorbate, the epimer of ascorbate was ineffective in generating the oxidative stress. These observations support the current concept that the high rates of dehydroascorbate transport via a GLUT after the release of ascorbate by glutamate leads to peroxidation, the role of glutamate on ascorbate/ dehydroascorbate recycling being critical to induce neuronal death via an oxidative stress in the brain injury.