초록 열기/닫기 버튼
Pro-oxidant properties of ascorbate have been studied with uses of brain tissues and neuronal cels. Here we address potential mechanism of ascorbate coupling with glutamate to generate ox-idative stres, and the role which oxidized as-corbate (dehydroascorbate) transport plays in oxi-dative neuronal injury. Ascorbate in neurones can be depleted by adding glutamate in culture med-ium since endogenous ascorbate can be ex-bate/dehydroascorbate transport by depleting as-corbate in the neurons with the glutamate-heter-oexchange. However, ascorbate is known readily being oxidized to dehydroascorbate in the med-ium. Glutamate enhanced the dehydroascorbate uptake by cels via a glucose transporter (GLUT) from extracelular region, and cytosolic dehydro-ascorbate enhanced lipid peroxide production and reduced glutathione (GSH) concentrations. Iso-as-corbate, the epimer of ascorbate was ineffective in generating the oxidative stress. These obser-vations support the curent 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 ascor-bate/dehydroascorbate recycling being critical to induce neuronal death via an oxidative stress in the brain injury.
키워드열기/닫기 버튼
ascorbate; glucose transporter; glutathione; lipid peroxide; neuronal death; oxidative stress
