[United theory of aging].

In attempts to develop a means of life prolongation the humankind has created more than three hundred theories of the aging; each of them offers the original cause of aging. However, none of them has given practical result by now. The majority of the theories have now only historical interest. There are several different theories that are mainly under consideration currently. They are based on reliable, proven evidence: the free radical theory, the protein error theory, the replicative senescence theory, the theory of reparation weakening, the immunological theory, several versions of neuroendocrinal theories, and programmed aging theory. The theory presented here is based on conception that the life as the phenomenon represents many of the interconnected physical and chemical processes propelled by energy of the mitochondrial bioenergetical machine. Gradual degradation of all vital processes is caused by the programmed decrease in level of bioenergetics. This theory unites all existing theories of aging constructed on authentic facts: it is shown, that such fundamental phenomena accompanying aging process as the increase in level of reactive oxygen species (ROS), the decrease in the general level of protein synthesis, the limitation of cellular dividing (Haiflick limit), decrease in efficiency of reparation mechanisms are caused by bioenergetics attenuation. Each of these phenomena in turn generates a number of harmful secondary processes. Any of the theories bases on one of these destructive phenomena or their combination. Hence, each of them describes one of sides of process of the aging initially caused by programmed decrease of level of bioenergetics. This united theory gives the chance to understand the nature of aging clock and explains a phenomenon of increase in longevity at the condition of food restriction. Failures of attempts to develop means from aging are explained by that the manipulations with the separate secondary phenomena of attenuation of bioenergetics, now in use, are not capable to advance longevity beyond the bounds of its natural duration. There is only one way to achieve an unlimited healthy life--to find a way of bioenergetics management.

[The mechanism of phenoptosis: I. Age-dependent decrease of the overall rate of protein synthesis is caused by the programmed attenuation of bio-energetics].

The age-dependent degradation of all vital processes of an organism can be result of influences of destructive factors (the stochastic mechanism of aging), or effect of realizations of the genetic program (phenoptosis). The stochastic free-radical theory of aging dominating now contradicts the set of empirical data, and the semicentenial attempts to create the means to slow down aging did not give any practical results. It makes obvious that the stochastic mechanism of aging is incorrect. At the same time, the alternative mechanism of the programmed aging is not developed yet but preconditions for it development have already been created. It is shown that the genes controlling process of aging exist (contrary to the customary opinion) and the increase in the level of damaged macromolecules (basic postulate of the free-radical theory) can be explained by programmed attenuation of bio-energetics. As the bio-energetics is a driving force of all vital processes, decrease of its level is capable to cause degradation of all functions of an organism. However to transform this postulate into a basis of the theory of phenoptosis it is necessary to show, that attenuation of bio-energetics predetermines such fundamental processes accompanying aging as decrease of the overall rate of protein biosynthesis, restriction of cellular proliferations (Hayflick limit), loss of telomeres etc. This article is the first step in this direction: the natural mechanism of interaction of overall rate of protein synthesis with a level of cellular bio-energetics is shown. This is built-in into the translation machine and based on dependence of recirculation rate of eukaryotic initiation factor 2 (elF2) from ATP/ADP value that is created by mitochondrial bio-energetic machine.

[Evolution mechanism of species-specific lifespan].

Numerous empiric data prove incontestably that species-specific lifespan is under control of genetic program. At the same time the modern evolution theories of aging deny an opportunity of existence of specific genes predetermining longevity. Basic premise for non-acceptance of the aging gene concept is convincing: animals in habitat do not live long enough for aging to exert any effect on their survival. Therefore, the natural selection can not differentiate them by the longevity attribute. To solve the collision the population approach was used in this work. As known from ecological laws the innate population growth rate (r(in)), lifetime of one generation (T), and inborn fertility (R(0)) are interconnected by the next dependence: r(in) = In R(0)/T. The examining of mathematical model of population showed that r(in) value is stabilized by inter-population natural selection on the level which corresponds to environment press in the species ecological niche. Therefore, species-specific longevity and fecundity are under control of this natural selection.

[The modified variant of mitochondrial theory of aging].

The central postulate of mitochondrial theory of aging (MTA) says that attenuation of cellular bioenergetics is the leading cause of aging. This attenuation is attributed to the accumulation of injuries into mitochondrial DNA that are exerted by reactive oxygen species (ROS). As the ROS are generated by mitochondrial respiratory chain then vicious cycle arises. As a result the ROS amount and level of injured biopolymers increase progressively and bioenergetics fades. The central postulate is fairly convincing but the mechanism of age-dependent bioenergetics attenuation is disproved by many empirical data. The new variant of MTA is suggested in this paper. According to this both the aging and the increase in ROS level are caused by the programmed bioenergetics fade. The mechanism of age-dependent increase in ROS is as follows. Superoxide radical (O2(*-)) generating by respiratory chain is neutralized in two stages: first the enzyme superoxide dismutase transforms O2(*-) into hydrogen peroxide and then H202 is converted into water and oxygen by glutathione peroxidase (GP). The reaction catalyzing by GP is shunted by Fenton reaction that produces extremely aggressive secondary radicals. The programmed bioenergetics decline decreases GP activity, which causes elevation of H202 content and increases hydrogen peroxide flow through Fenton reaction. This leads to the increase in general ROS level and to strengthening their aggressivity. Thus, both the aging and the increase in ROS level are two consequences of programmed bioenergetics decline.

Effect of actinomycin D on tobacco mosaic virus (TMV) accumulation in isolated tobacco protoplasts under varying light conditions.

The effect on Tobacco mosaic virus (TMV) accumulation of actinomycin D (AMD) introduced shortly after inoculation into isolated tobacco protoplasts under varying light conditions was examined. The emission spectrum of the light source contained lines in the visible range and in the ultraviolet band (300-400 nm). AMD absorbed light in the visible (400-500 nm) and in the uv (200-400 nm) ranges. AMD substantially inhibited TMV multiplication in the light, and also when the protoplasts were incubated in petri dishes covered with a black filter that allowed only uv light in the range 260-390 nm to pass. In the dark, and also in petri dishes covered with blue or yellow filters that passed in the ranges 400-500 or 500-600 nm, respectively, AMD stimulated TMV reproduction. The suppression of TMV multiplication in isolated tobacco protoplasts was assumed to be associated with a photodynamic effect caused by absorption of uv light by AMD.