Researches of radioinduced life span alteration of Drosophila which is carried out in our laboratory in 1996-2003 years, have revealed interrelation between mutations of several genes of DNA repair and apoptosis pathways with low doses ionizing irradiation and speed of aging.
It was used Drosophila individuals, developing in conditions of a chronic low dose irradiation or on nutrition medium with apoptosis inducer etoposide addition. The exposition doze was 0.17 sGy/h. The absorbed doze for one generation (from an embrio stage up to an imago start, 10-12 days) corresponded 60 sGy. Etoposide treatment carried out on preimago stages (5 mkM in a nutrient medium n concentration).
We investigated the life span after irradiation and etoposide treatment of Drosophila melanogaster laboratory populations with defects of some genes of DNA repair machinery and apoptosis pathways in homozygous and heterozygous state, such as mei-41 (ATM homolog), two alleles of Dcp-1 (Drosophila caspase), dArk (Apaf-1 homolog), rpr, grim, hid, three alleles of th (IAP homolog), wg (Wnt family member). It is shown, that the irradiation and etoposide treatment of these strains results in life span change depending on a genotype of the investigated line. The results will be considering in the report.
As well, the analysis of age - dependent change of nervous system activity (as the test of aging speed) of Drosophila melanogaster imago was carried out. It was shown, that the irradiation of strains with the increased apoptosis sensitivity results in elevated nervous - muscular activity of imago during all experiment periods. At th1 strain increase of activity in comparison with the control in the first week has made 41 %, and in two subsequent - about 80 %. Last week authentic increase did not observe. At th4 strain statistically significant increase of activity in comparison with the control observed in the first week of experiment (18 %), in the second (67 %) and the fourth (88 %). The irradiation of a wild type strain Berlin has caused authentic increase of activity in comparison with the control for the thirteenth day (on 17 %) and for the twentieth day (37 %). At the same time, at strains with the lowered sensitivity to apoptosis: at strain which individuals are heterozygous in deletion of proapoptosis genes rpr, grim and hid; at strains with dysfunction of proapoptosis gene dArk; at strains with dysfunction of caspase Dcp-1 (Dcp-102132 and Dcp-1k05606 allels) authentic changes of nervous - muscular activity it was not shown.
Thus, we observed the delayed role of apoptosis induction on ageing speed.