The small doses of radiation can increase the likelihood of developing cancer [Brenner

D. J., Doll R. & Goodhead D. T. 2003, NCR 2006] and is possibility appearing morbidity non-cancer origin [Hildebrandt G. 2010]. The main outcome of the 25-year study of morbidity in different categories of exposed persons in connection with the Chernobyl catastrophe is a significant increase in primary morbidity is not associated with tumor pathology. Not found increased risk of leukemia even among those engaged in reconstruction work. Only recently become apparent relationship of radiation exposure with increasing number of non-oncological pathology such as cardiovascular diseases [Preston D. L, Shimuzu Y. & Pierce D. A. 2003]

Statistically significant increase in the spread of non-neoplastic diseases is shown in [Bouzounov O. V., Tereshchenko V. M. 2010]. At the same time structure of morbidity leading place is occupied by diseases of digestive, circulatory and nervous system The maximum level and the largest number with the non-neoplastic diseases statistically confirmed by link determined in the dose > 0,25 Gy for subcohort study group. Long-term effects of chronic low-intensity exposure to low doses for exposed persons in this category until the end is unclear.

The rapid growth of non-tumor morbidity in exposed populations reflects certain changes in the systems that control the growth, development and aging, namely stereotypes matching sequence and intensity of reading the genetic information in different cells. It is shown that this task cannot perform any neural mechanism, or hormonal agents with their ability to alter the rate of metabolic processes. Neurotransmitters, hormones and their receptors do not possess sufficient ontogenetic variability and dispersal [Poletayev A. B. 2008].

According to modern ideas exactly a physiological autoimmunity throughout life provides a readout of genetic information in different cells of the whole organism [Churilov L. P. 2008, Maltsev V. N. 1983, Zaichik A. Sh. & Churilov L. P. 2008]. Singularity of the function of autoantibodies (AuAB) compared with other regulatory substances is considerably longer their half-lives ranged from 10 to 50 days. Therefore the system of autoimmunity has greater inertia. Autoantibodies regulate slow the physiological processes that continue some days and weeks [Ashmarin I. P., Freidlin V. P. 2005]. It is postulated that a mild autoimmune response to their own antigens is a necessary condition for the normal functioning of the immune system and is a prerequisite for the normal regulation and synchronization of cellular functions and morphogenesis [Churilov L. P. 2008]. Additional conditions for unmasking antigens of tissues and organs and represent them immune cells with subsequent increased production of specific AuAB appear as a result of exposure to ionizing radiation.

It is well known that oxygen absorbed by the mitochondria is converted into adenosine triphosphoric acid (ATP). About 5% of oxygen consumed by tissues is converted into free radicals such as superoxide, hydrogen peroxide, hydroxyl radical, singlet oxygen, peroxynitrite (reactive oxygen species, ROC) with unpaired valence electrons. Most of the ROS are produced continuously in cells as byproducts of normal cellular metabolism (mainly due to a small leakage of electrons to the mitochondrial respiratory chain, as well as other reactions in the cytoplasm), and do not cause damage to cells. An excess of ROS under intense ionizing radiation exceeds the protective capabilities cells and can cause serious cell disorders (eg, depletion of ATP). The increase of free radical molecules and their products have a place in the development of the state of homeostasis, has been called oxidative stress. Slow development of oxidative stress triggers apoptosis, and its intensive development leads to necrosis. Postradiation apoptosis is characterized by maintaining the integrity of the cell plasma membrane and the lack of exposure of intracellular contents from cells of the immune system. In the end, remnants of apoptotic cells are removed by exfoliation in intraorganic space and subsequently excreted from the body. But the shortage of ATP, in particular after irradiation, the energy dependence of the mechanisms of apoptosis are disabled, and the cell dies with loss of cell membrane integrity and release of macromolecular components (eg, ALT, AST, etc.) into the intercellular space. Necrosis caused an immune response in the form of inflammation — leukocyte infiltration of the affected tissue, interstitial fluid accumulation and subsequent induction of specific immune responses (specifically sensibilized T-lymphocytes and autoantibodies) to the unmasked and recognized by lymphocytes of intracellular components. According to data of many researchers the AuAB are primarily the attribute of the norm. They can be identified in healthy individuals. [Churilov L. P. 2008, Zaichik A. Sh. & Churilov L. P. 2008b, Poletayev A. B. 2005, Cohen I. R. 2005, Harel M. & Shoenfeld Y. 2006, Shoenfeld Y. 2008]. The AuAB involved in the process of apoptosis, cleaning the body from catabolic products, modulation of the activity of many enzymes and hormones, as well as perform the transport function [Poletayev A. B. 2008a]. It was shown that antibodies against nuclear antigens can penetrate into the cell nucleus in vivo and stimulate the synthesis of RNA and DNA in target cells [Zaichik A. Sh. & Churilov L. P. 1988].

Notkins in 2007 hypothesized that natural AuAB can be very informative not only precursors of autoimmune diseases, but also a variety of somatic diseases and syndromes [Notkins A. L. 2007]. It is important that changes in the content of organ natural AuAT in most cases, ahead of the clinical manifestation of appropriate forms of pathology. If for example the content of "cardiotropic", hepatotropic", "neurotropic" AuAB a concrete person within the borders of the norm, this suggests that the intensity of apoptosis, respectively, cells of the heart, liver or nerve tissue does not go beyond the norm. Persistent changes, for example, from "hepatotropic" AuAB should be regarded as a sign of the possible formation of a pathological process in liver tissue, even if at the time of examination are no clear clinical symptoms or specific biochemical changes [Poletayev A. B. 2008a, Churilov L. P. 2008, Notkins A. L. 2007, Zedman, A. J.W. & Vossenaar E. R. 2004].

The important role of the abolition of immune tolerance in the occurrence of non-viral hepatitis research shows serum levels of antibodies to liver-specific lipoprotein (LSP) for various categories of people. [Kovalev V. A. & Senyuk O. F., 2008].

The LSP which was first isolated by Meyer zum Burschenfelde and Miescher in 1971 is considered to be specific poly antigen for the liver. Native LSP is mixture of antigenic determinants of the substrate from the membranes of hepatocytes and contains soluble and membrane components were isolated by gel filtration (chromatography) supernatant after ultra — centrifugation of liver homogenate [Manns M, Gerken G. & Kyriatsoulis A, 1987, Ballot

E. , Homberg J. C. & Johanet C. 2000]. It is known that LSP is found not only in the liver, but also in some other organs [Garcia-Buey., Garcia-Monzon C. & Rodriguez S. 1995]. Therefore, the total increase in antibody levels to the PSL can be seen as a sign of abolition of immune tolerance to many organs and tissues of the human body [Kovalev V. A. & Seniuk O. F., 2008].

There are three outcomes for the cell, if the cellular radiation damage is not adequately repaired. The cell may die, or will delay it or keep playing with the viability of new qualities, or mutations as the basis for the development of remote descendants (See figure 17). The consequences of the first approach in the development of cells after irradiation described below.

The linear non-threshold concept is used as the primary standard for radiation protection and risk assessment for many years. It suggests that damage induced by low doses of radiation do not contribute significantly to increased risk of disease because a significant amount of endogenous genome damage occurs during life and they are restored in cells with high probably. In fact endogenous damages (ED) constantly appear in the cells. Some of them are due to thermodynamic processes, the hydrolysis reaction, while others arise from the effects of free radicals generated by cell during its life and still others are a necessary component of metabolism (DNA breaks accompany the process of differentiation, recombination, etc.) [Lindahl T. 1993, Bont R. D. & Van Larebeke N. 2004]. According to [Lindahl T., 1993] per one day in the DNA of one cell may have more than 50,000 endogenous damages as single-strand breaks (SSB) and 10 ones as double-strand breaks (DSB).

Many studies suggest that most of the radiation damage (RD) occurring in the DNA of cells differ significantly in their chemical nature from the ED. The main difference between DNA damage induced by ionizing radiation, from the ED was its the complexity of their chemical nature, and clustering. The proportion of complex, critical for the fate of the cell damage is much higher when exposed to IR.

When treatment of mammalian cells to H2O2 ratio of DSB to SSB is 1: 10 000 [Bradley M. O. & Kohn K. W. 1979] while under the influence of IR is much higher -1:20 [Shikazono N., Noguchi M., & Fujii K. 2009]. Many of the DNA RD are not accidental, are located in close proximity and have the cluster grouping. They are formed as a result of coincidence of two or more single damages within 1-2 rotation the DNA helix [Hada M., Georgakilas A. C. 2008, Sutherland B. M., Bennet P. V. & Sidorkina O. 2000]. Especially the massive clustering of DNA damage occurs when the ionization tracks pass along chromatin fiber. In this case, they may cover DNA regions with an average size of about 2000 base pairs [Radulescu I., Elmroth K. & Stenerlow B. 2004]. At the same time, we know that the probability of occurrence of endogenous clustered DNA damage is extremely low [Bennett P. V., Cintron N. S. & Gros L. 2004]. Accumulation of ED does not occur because in the cells are constantly functioning mechanisms of reparation, specifically targeted at removing various types damages [Friedburg E. C., Walker G. C. & Siede W. 2006].

The complex nature of RD of DNA and the presence of cluster groups can be regarded as the first cause, which creates difficulties for repairing systems cells. Damages repair processes within the cluster can break down in various stages of excision repair and lead to the formation of additional or inaccurate DSB repair, important for cell survival, mutagenesis, and the risk of malignancy [Ide H., Shoulkamy M. I. & Nakano T. 2010]. The second reason for the low efficiency of repair of RD may be a relatively low amount of DNA damage. Therefore, radiation effects in low dose range and low power are certain features associated not only with destructive modifications but with deducing the cellular genome at a different level of activity. High doses of ionizing radiation via activation of cell cycle control points — checkpoints, blocking the synthetic phase of the cell cycle (S) and the transition from G1 to S phase and G2 to M (mitotic) phase and support the repair of DNA. In this case, small doses can not activate the G2/M chekpoynt-arrest and DNA repair are not activated when the number of DSB DNA damage and the MNF up to 10 — 20 per cell.

In this case, heterochromatin little relaxes, and access of repair enzymes to sites of DNA damage worsens [Fernet M, Megnin-Chanet F. & Hall J. 2010, Grudzenskia S., Rathsa A., Conrada S., 2010, Marples B., Wouters B. G. & Collis S. J. 2004, Gaziyev A. I. 2011]. There is the third of the possible causes of low efficiency of repair of critical DNA damages.

The major part of radiation induced DNA damages are represented by DSB and crosslink between strands, which slowly and inefficiently repaired and are responsible for various end effects — from the radiation death of cells to the appearance of chromosome aberration, gene mutations and neoplastic transformation. [Pfeiffer P., Gottlich B. & Reichenberger S. 1996]. Therefore radiation effects in low dose range and low rate dose have the certain features associated not only with destructive changes than with deducing the cellular genome at another level of activity. Analysis of many studies suggests that DNA damage caused by the IR, increase linearly with dose, but the reaction of cells on these lesions, the efficiency of repair of the most complicated critical damages can be nonlinear. Because irradiation is decreased expression of proteins, enzymes of different systems providing the stability of DNA as a result of the accumulation of DNA damage is not recovered or recovered with errors and fix mutations. Dysfunction of many genes, regulatory systems and cellular processes that are ultimately linked to the development of various pathologies, including carcinogenesis. A significant part of replication errors — spontaneous mutations — can be harmful to an organism. There are the basis for the occurrence of hereditary diseases, carcinogenesis, etc. were revealed.