Abstract
Impairment of long-term memory is characteristic of aging and some neurodegenerative diseases associated with the increased generation of reactive oxygen species (ROS). An inbred OXYS rat strain was developed from Wistar rats with an inherited overproduction of ROS, manifesting impairment of long-term memory and oxidative damage of cell structures and functions. A highly inbred OYXR strain harboring oxidative patterns close to normal Wistar rats served as a control. Alterations of brain neurochemical functions in OXYS rats and the possibility of protecting them with different antioxidants were studied. Assaying the oxidative DNA lesion, 8-hydroxydeoxyguanine (8-OHdG), and lipid peroxidation-induced etheno-DNA adducts in rat liver DNA indicated a high oxidative stress in OXYS rats. We found that the Na/K-ATPase activity, N-methyl-D-aspartate (NMDA) receptors, and the integrity of sulfhydryl (SH) groups, parameters associated with memory-related neurochemical mechanisms, were altered in OXYS rat brains compared to that of control OXYR rats. Protection of neurochemical functions was investigated by long-term treatment of OXYS rats with different antioxidants, namely, 2,6-di-tert-butyl-4-methylphenol (butylated hydroxytoluene; BHT), 2,6-dimethyl-3-hydroxypyridine (emoxipine), and β-alanyl-L-histidine (carnosine). We determined that BHT protected rat brains from the oxidative alteration of Na/K-ATPase but did not protect NMDA receptors and SH groups. Emoxipine protected rat brain from oxidative impairment of SH group, but did not protect NMDA receptors and Na/K-ATPase. Carnosine protected from oxidative impairment rat brain NMDA receptors, Na/K-ATPase, and protein SH groups.
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