Senescence as morbus reponibilis
A.V. Khalyavkin, A.I. Yashin
Institute of Biochemical Physics of RAS, 4, Kosygin Street, Moscow GSP-1, 119991, Russia; Duke University, NC, USA
At the moment there is no conclusion on the origin of senescence.
Recently the author of a telomere shrinkage hypothesis of aging has
rejected it as explanation of an origin of aging and has put forward a
new one (Olovnikov, Biochemistry 2003; Adv.Gerontol. 2003). On the
other hand, one of the most commonly noted versions of the free radical
theory of aging has also failed to explain non-pathological senescence
(Orr, Sohal, Exp.Gerontol. 2003). Moreover, recent studies have
implicated reactive oxygen species (ROS) as natural second messengers
contributing to signal transduction involved in gene transcription
control. The rate of ROS generation in cells is under strict control of
several hormones, cytokines, and growth factors. As the role of
signaling in aging control is very important (Cell 2005;120:449) we
propose the view that the organism's senescence is controlled by cues
received from the environment. We suppose that natural aging stems from
an inevitable shift in certain parameters of physiological control
systems under the influence of inadequate environmental conditions,
which are not able fully to induce the organism's optimal existence in
the self-maintenance mode. In this case the rate of aging is
proportional to the multidimensional difference between cues from the
evolutionarily designed adequate habitat and signals from the real
environment. The negative correlation between the parameters of
Gompertzian mortality (among other findings) is compatible with this
view. Artificial stimulation of control systems can reduce a deficit of
these adequate environmental signals. Therefore different external cues
can either evoke senescence or even reverse aging manifestations.
Key words:
aging plasticity, external influences, aging reversibility
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