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», 2013,
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,
13. Probst L.E.,Halfaker J.S.,Holland E.J.,1997.Quality of corneal
donor tissue in the greather-than-75-year age group // Cornea V.16.P. 507511.
: 0,014 %
(
., 2003).
.
,
Resume
TISSUES GET OLD WITHOUT AGEING OF CELLS:
THE UNIVERSAL MECHANISM OF AGEING
Artemov A.V.
.
1.
.,
.
., 2003.
-
//
.4. .2. .73-75.
., 2007.
.
:
. 186 .
3.
., 2003.
.
.664 .
4.
., 1966.
.:
. 300 .
5.
., 2007.
:
//
.68. 1. .19-24
6.
.,
., 1999.
.
.184 .
7.
.,1988.
.:
. 239 .
8. Gatti S., 2002.The role of sponges in high-Antarctic carbon and
silicon cycling: a modellling approach // lfred Wegener Institute for Polar
and Marine Research: Bremerhaven.
9. Kerr J.F.,Wyllie A.H.,Currie A.R., 1972.Apoptosis: a basic
biological phenomenon with wide-ranging implication in the tissue kinetics
// Brit.J.Cancer V.26.P.239-57.
10. Mishima S., 1982. Clinical investigation of the corneal
endothelium //Amer.J.Ophthalmol.V.93. P.1-29.
11. uller-Pedersen T.,1997. A comparative study of human
corneal keratocyte and endothelial cell density during ageing //Cornea V.16.
P.333-338.
12. Murphy C.,Alvarado J.,Juster R.,Maglio M,.1984. Prenatal and
postnatal cellularity of the human corneal endothelium: a quantitative
histologic study// Invest.Ophthalmol.Vis.Sci.V.25.P.312-322
2.
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. 135
The modern gerontology explains ageing of the multicellular
organisms by ageing of cells as a result of accumulation of errors in
genome. However, the mechanism of accumulation of damages is not
found and theoretically is not predicted till now. At the same time,
ageing, that is imperceptible at the level of separate cells and its genome,
is shown at the level of tissues as a reduction of number of cells. This
morphological fact is known for a long time. It is explained by cell
ageing and subsequent death of cells.
Morphological studying of the age changes of corneal
endothelium has allowed to pay attention for the first time to the major
circumstance: loss of cells in tissue is not increasing during life, i.e. it
cannot be a consequence of cell ageing. This age-independent process
refutes the existent representation. The functional weakness of tissues
with the years is a result of casual death of cells.
A regular stochastic destruction of cells can be caused by
random errors at the level of transcription and translation. So, it is
known that genome is a subject to the mutational noise. The point
mutations arise at each act of reparation. They can repeat, but they are
not collected and cannot lead to genome ageing. However, mutational
noise contains risk of occurrence of lethal mutations. For example,
repeated error in synthesis of proteins, providing contact of cell with
matrix, initiates membrane-mediated apoptosis and destruction of cells
in the tissue systems. Reduction of cells leads to loss of functionality of
tissues. It is accompanied by functional easing at the system level. So,
through casual death of cells there is a degradation of tissues as a result
of reduction of the cell number.
Thus, ageing is a stochastic destruction of cells in tissues as a
result of information error in a protein synthesis. Organism ageing is an
», 2013,
1-12,
. 136
ageing of tissues that happens without ageing of cells. It is result of
information instability of genome and not a consequence of its age
degradation.
Artemov A.V., Ph.D
Chairman of the Department of Eye Pathology and
Preservation of Donor Tissues.
The Filatov Institute of Eye Diseases and Tissue Therapy
French boulevard, 49/51.
Odessa, Ukraine, 65061
9
2012 .
,
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el.mail: art_onkol@ukr.net
», 2013,
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. 137