Abstract
Ontogenetic differences in the rate of apoptosis and expression of apoptosis signal proteins, as well as in the effects of the antioxidant α-tocopherol acetate on the neurons of magnocellular hypothalamic centers in BALB-c mice under stress were revealed. Hypohydration stress was found to initiate neuron apoptosis in both young and old animals. The stress-protective effects of α-tocopherol acetate were more pronounced in young animals. The following tendencies were established in the course of immunohistochemical studies of pro- and antiapoptotic protein expression. Dehydration results in increased synthesis of the proapoptotic protein Bax in neurosecretory cells of the hypothalamus in young mice and decreases the antiapoptotic effect of the proteins of the Bcl-2 family independently of the animal’s age, thus promoting neuron death. Apparently, the more pronounced antiapoptotic effect of α-tocopherol acetate in young mice under stress, if compared to elderly animals, is due to the rapid induction of compensatory mechanisms, namely, a decrease in the synthesis of the proapoptotic proteins p53 and Bax and increase in the expression of the antiapoptotic protein Bcl-2.
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Original Russian Text © Yu.V. Azizova, D.L. Teplyi, E.D. Bazhanova, O.N. Pozdnyakova, 2011, published in Uspekhi Gerontologii, 2011, Vol. 24, No. 2, pp. 220–224.
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Azizova, Y.V., Teplyi, D.L., Bazhanova, E.D. et al. The effect of water deprivation and α-tocopherol acetate on the expression of apoptosis marker proteins. Adv Gerontol 2, 38–42 (2012). https://doi.org/10.1134/S2079057012010031
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DOI: https://doi.org/10.1134/S2079057012010031