Epigenetic Variations in Chromatin Caused by the Combination of Bioregulators with Heavy Metals During Aging

The aim of this study was to determine the level of chromatin condensation, the frequency of chromosomal aberrations and sister chromatid exchanges, based on the actions of bioregulators Livagen -( Lys-Glu-Asp-Ala) and Epitalon - (Ala-Glu-Asp-Glyin), and metal ions - Nickel, Cobalt and Zinc their se...

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Veröffentlicht in:International journal of peptide research and therapeutics 2022-07, Vol.28 (4), Article 121
Hauptverfasser: Lezhava, Teimuraz, Jokhadze, Tinatin, Monaselidze, Jamlet, Buadze, Tamar, Gaiozishvili, Maia, Sigua, Tamar, Chigvinadze, Nino, Kilaberia, Ekaterine
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Sprache:eng
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Zusammenfassung:The aim of this study was to determine the level of chromatin condensation, the frequency of chromosomal aberrations and sister chromatid exchanges, based on the actions of bioregulators Livagen -( Lys-Glu-Asp-Ala) and Epitalon - (Ala-Glu-Asp-Glyin), and metal ions - Nickel, Cobalt and Zinc their separate and combined effects in cultivated lymphocytes of 20-40- and 71-86-year-old healthy individuals. The analysis of results shows the chromosome progressive heterochromatinization (condensation of eu- and heterochromatin regions) occur in aging. The Livagen and Epitalon in the lymphocytes of senile individuals unfold the highest level of chromatin, releasing of genes inactivated, indicates their ability to modify chromatin towards deheterochromatinization. Used bioregulators - Livagen and Epitalon showed a pronounced anti-mutagenic - protective effect in both age groups, reducing the metals ions (Cobalt, Nickel and Zinc) ability to induce high frequency of cells with chromosomal aberrations. The obtained data indicates that short peptides Livagen and Epitalon, and metal ions (Nickel, Cobalt, Zinc) with their separate and combined action, cause selective epigenetic variability, heterochromatinization and deheterochromatinization of chromatin in persons 71–86 years old, that opens up new opportunities for research that can lead to therapeutic interventions aimed at anti-mutagenic action and selective activation of inactive genes in heterochromatinized areas.
ISSN:1573-3904
1573-3149
1573-3904
DOI:10.1007/s10989-022-10427-9