THE PRESENCE OF CALBINDIN IN RAT CORTICAL-NEURONS PROTECTS IN-VITRO FROM OXIDATIVE STRESS

Free radicals are highly reactive chemicals containing an unpaired ele ctron and are normally produced by the cellular metabolism. The oxydat ive stress is defined as a lack of balance between the production of f ree radicals and the activity of antioxydant metabolites. It induces c ellular damages to lipids, proteins and membranes. Abnormal calcium me tabolism can be a consequence of oxydative stress leading to increased intracellular concentrations. Calbindin D28K is a calcium binding pro tein which could have a neuroprotective action against various cellula r insults. In this study rat cortical cell cultures were exposed durin g various times and at different concentrations to the couple Xanthine /Xanthine oxydase (XA/XO), which produces the superoxyde radical O-2(_ ). Neuronal survival revealed that XA/XO is toxic for cortical cell cu ltures. The Calbindin D-28k immunocytochemical study shows that the pe rcentages of Calbindin positive cells are greater in surviving neurons following the XA/XO exposure compared to controls. There is a time-de pendent and a dose-dependent relation between the number of surviving neurons and the percentage of Calbindin positive neurons. These result s suggest that the presence of cytosolic neuronal Calbindin D-28k is a ssociated with a greater resistance to oxydative stress.