ABSTRACT
Short arms, satellite stalks and satellites of human acrocentric chromosomes (13, 14, 15, 21 and 22) represent heterochromatic regions. Enforced by mutual attraction of heterochromatic regions, the short arms of acrocentric chromosomes come close to each other and compose associations. The associations of human acrocentric chromosomes cause nucleolus formation, undergo age-related changes, account for elevated incidence of chromosome rearrangements and, consequently, can cause chromosome diseases. Most acrocentric chromosome associations are formed by chromatid satellite stalks. This work contains results of acrocentric association rates assessed with use of newly designed mathematical model, which is based on two parameters: the probability of formation and the association intensity for different acrocentric chromosome pairs. For middle-aged individuals the following values were defined: S(0) = 0.558, lambda(V) = 0.2706, lambda(V) = 0.4768 and lambda(W) = 0.0960. The new mathematical model for satellite associations makes it possible to compare two cells not only by the total number of acrocentric chromosome associations, but also by the type and character of each association.
Subject(s)
Centromere/genetics , Chromosomes, Human/genetics , DNA, Satellite/genetics , Models, Genetic , HumansABSTRACT
Effect of aging on adaptive response of cellular systems to low (stimulated) dozes of gamma-rays (0, 2 and 0, 5 Gy) and to disturbing dozes of radiation (1 and 2 Gy) has been investigated. PHA-stimulated cells were from 72-86 year-old individuals; control - 30-40 year-old individuals. The potentialities of induction of adaptive response in cells exposed to previously irradiated by stimulating dozes of gamma-rays with subsequent damaging effect of copper chloride (10(-3)M) has been investigated. The correcting activity of the peptide bioregulator Livagen was tested. The investigation showed that cells from aged individuals maintained radiation adaptive feature. Preliminary exposure to radiation caused stimulation of adaptive response in copper-treated cells. Corrective activity of Livagen was observed.
Subject(s)
Adaptation, Physiological/drug effects , Aging/physiology , Oligopeptides/pharmacology , Radiation Tolerance/drug effects , Radiation-Protective Agents/pharmacology , Adaptation, Physiological/radiation effects , Aged , Aged, 80 and over , Female , Gamma Rays , Humans , Lymphocytes/drug effects , Lymphocytes/radiation effects , MaleABSTRACT
The effect of synthetic peptide bioregulators (Epitalon, Livagen and Vilon) on structural and facultative heterochromatin of cultivated lymphocytes have been studied among old (75-88yr.) people. The data obtained indicate that epitalon, livagen and vilon: 1) activate synthetic processes, caused by reactivation of ribosomal genes as a result of deheterochromatinization (decondensation) of nucleolus organizer regions; 2) induce unrolling (deheterochromatinization) of total heterochromatin; 3) release genes repressed by heterochromatinization (condensation) of euchromatic regions forming facultative heterochromatin; 4) epitalon and livagen induce deheterochromatinization (decondensation) of pericentromeric structural heterochromatin of the chromosomes1 and 9. However, vilon does not induce deheterochromatinization of pericentromeric structural heterochromatin. These results indicate that peptide bioregulators Epitalon, Livagen and Vilon cause activation (deheterochromatinization) of chromatin in lymphocytes of old individuals.
Subject(s)
Aging/drug effects , Chromatin/metabolism , Dipeptides/pharmacology , Oligopeptides/pharmacology , Biodegradation, Environmental/drug effects , HumansABSTRACT
We studied the effects of the synthetic peptide Livagen on activity of ribosomal genes, denaturation parameters of heterochromatin, polymorphism of structural C-heterochromatin, and variability of facultative heterochromatin in lymphocytes from old people. Livagen induced activation of ribosomal genes, decondensation of pericentromeric structural heterochromatin, and release of genes repressed due to age-related condensation of euchromatic regions in chromosomes. Our results indicate that Livagen causes de-heterochromatinization (activation) of chromatin, which is realized via modification of heterochromatin and heterochromatinized regions in chromosomes from old people.
