CONICET | Buscador de Institutos y Recursos Humanos

Developing Central Nervous System (CNS) is vulnerable to radiation-induced reactive oxygen species. The consequent oxidative stress has been shown to produce changes at different levels in the hippocampus, involving the participation of different molecular targets. The aim of the present work was to evaluate the participation of PKC -a protein involved in the memory mechanism- in the changes induced by X radiation and the ability of 17βestradiol (βE), a potential neuroprotector, to counteract these effects. Neonatal male Wistar rats were X-irradiated (5 Gy) in their cephalic ends up to 48hs of postnatal life and a group of these animals (E2) was treated with 17β-estradiol (5 μg/g). Inhibitory avoidance (IA) and Elevated Plus Maze (EPM) tests as well as the levels of PKC (total activity and protein quantity of β1 isoform) were determined in the hippocampus of 30-days-old rats. In the IA test, the irradiated group (Rx) showed an improvement in the performance that was not reversed by ßE. However, βE was able to restore the decrease in anxiety observed in the Rx group. The PKC activity was increased in the Rx group and remained increased in the E2 group; although a decrease in the PKC traslocation to the membrane was induced in E2 group. On the other hand, the protein quantification of the β1 isoform showed a tendency to increase in the Rx group that was partially restored with βE treatment. A group of additional experiments of protein quantification to demonstrate the statistical significance are currently in course. These results suggest that PKC have an important role in the changes induced by X-rays on the hippocampus. This enzyme would be implicated in the better performance of the Rx group as well as in the modification in the anxiety levels. On the other hand, the present work demonstrated that βE was able to counteract, at least in part, radiation-induced changes, probably acting on molecular targets like PKC.