ABSTRACT
We revealed ontogenetic features in apoptosis level, apoptosis signal proteins expression, antioxidant (alpha-tocoferoli acetate) effects in neurons of magnocellular hypothalamic centers of BALB-c mice. It was obtained that water deprivation stress leads to apoptosis initiation of neurons in both age groups. Stress-protected action of alpha-tocoferoli acetate was more significantly in young mice compared to old ones. In our subsequent work (immunocytochemical reactions) we obtained further regular occurrences. Dehydration leads to increase of proapoptotic protein Bax synthesis in hypothalamic neurosecretory cells in young mice and in age-independent manner, this stress leads to decrease of antiapoptotic proteins Bcl-2 and Mcl-1 synthesis. So, the apoptosis level increases. More significant antiapoptotic action of alpha-tocoferoli acetate in stress condition in young mice is obviously connected with quick reaction of compensatory mechanisms (low expression of proapoptotic proteins p53, Bax and high expression of antiapoptotic protein Bcl-2).
