PARENT SESSION
Work-in-Progress
(WIP-385) Free radical production and oxidative stress in the brain after ionizing radiation.
Kim, Yun-Jeong1, Sung, Jae-Suk1, Park, Ji-Sun1, Park, Eun-Mi1, Kim, Dae-Joong2, Park, Young-Mee*,1, 1 Division of Chemistry and Biology, Incheon, Korea2 Department of Anatomy, College of Medicine, Incheon, Korea
ABSTRACT-
Oxidative stress has been implicated as in the various forms of brain disease and tissue damage. While a critical role of oxygen-derived free radicals has been implicated in radiation-induced tissue damage, oxidative consequences of the irradiated brain are not well understood. In this study, mice were irradiated and the brains were analyzed for oxidative stress. Our data show a significant increase of free radical formation, glutathione depletion, and lipid peroxidation in the irradiated brain, which was accompanied by the NFkB and AP-1 activation. Evidence that a pretreatment with a divalent cation chelator increased the NFkB and AP-1 activation indicated that ROS formation via a Fenton-type reaction is involved the radiation-induced NFkB and AP-1 activation in the brain. That the pretreatment of glutathione depleting agent, buthionine sulfoximine significantly increased NFkB and AP-1 activation strongly indicated an important role of glutathione in modulating the oxidative stress in the brain. [Supported by a grant from MOST]
KEYWORDS: Radiation, Reactive Oxygen Species (ROS), NF-kappaB, AP-1