ADAPTATION OF CELLS IN THEIR DAMAGE

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Action on the cell pathogens naturally accompanied by the activation (or inclusion) of reactions aimed at eliminating any decrease in the degree of damage and its consequences. The complex of these reactions provide a device (adaptation) of the cell to change its conditions of life. The major reactions include adaptive compensation mechanisms, recovery of lost or damaged substitution patterns and impaired functions, protect cells from the effects of pathogenic agents and functional decline in their regulatory activity. All complex adaptive responses can be divided into two groups: the intracellular and intercellular.

Intracellular adaptive mechanisms in case of damage. The following can be attributed to one of them.

Mechanisms of adaptation of cells when they are damaged

1. Payment of violations energy supply of cells:

- Intensification of re-synthesis of ATP during glycolysis and tissue respiration in intact mitochondria

- Activation of ATP energy transport mechanisms

- Activation of ATP energy recovery mechanisms.

2. Protection of cell membranes and enzymes:

- Increase in the activity of antioxidant defense system factors

- Activation of the buffer systems,

- Increase in the activity of detoxification enzymes microsomes

- Activation of the mechanisms of repair components of membranes and enzymes.

3. Reducing or eliminating the imbalance in ion and fluid cells:

- Reducing the degree of disturbance of energy,

- Reduction of the degree of damage to the membranes and enzymes,

- Activation of the buffer systems.

4. Fix Violations cell genetic program:

- The elimination of gaps in the strands of DNA,

- The elimination of (block) the modified DNA segments,

- Synthesis of normal DNA fragment instead of damaged or lost.

5. Payment disorders mechanisms regulating intracellular processes:

- Changes in the number of "functioning" of the cell receptors,

- Change the cell receptor affinity to regulatory factors,

- Changes in activity of adenylate - and (or) guanylate cyclase systems and other "intermediary" systems,

- Change in the activity and (or) the content of intracellular metabolism regulators (enzymes etc. cations.).

Reducing the functional activity of the cells.

1. Regeneration.

2. Hypertrophy.

3. Hyperplasia.

Compensation violations energy supply of cells. If damaged cells tend to be more or less affected mitochondria and reduced ATP resynthesis in tissue respiration process. It serves as a signal to increase the ATP "products" in the glycolysis system. With a weak or moderate damage to the activation of ATP re-synthesis can be achieved by increasing the activity of enzymes involved in the processes of oxidation and phosphorylation.

Some contribution to the compensation of disturbances of intracellular processes of power supply in case of damage makes the activation of enzymes transport and utilization of ATP energy (creatine kinase, ATPase), and also limit the functionality of cell activation. The latter contributes to a substantial reduction of energy consumption of ATP.

Protecting cell membranes and enzymes. One of the most important mechanisms of damage to the membrane unit cells and enzymes is the intensification of free radical and peroxide reactions. The intensity of these reactions is limited mostly antioxidant enzymes - superoxide dismutase (inactivating O2 radicals), catalase and glutathione peroxidase that break down hydrogen peroxide, respectively, and lipids.

Another mechanism of protection of the membrane and the damaging action of enzymes, in particular lysosomal enzyme can be activated cell buffer systems. This causes a decrease in the degree of intracellular acidosis and as a result of excessive activity of the hydrolytic lysosomal enzymes.

An important role in protecting cell membranes and enzymes from damage play microsomal enzymes (primarily endoplasmic reticulum), providing a physical and chemical transformation of pathogenic agents by oxidation, reduction, demethylation, etc. Alteration of cells may be followed by derepression of genes and thus activating the synthesis and repair of membrane components (proteins, lipids, carbohydrates) to replace damaged or lost.

Reducing or eliminating the imbalance in ion and fluid cells. If damaged cells eliminate the imbalance of ions and fluid can be achieved by activating the mechanisms of energy supply ion "pumps", as well as the protection of membranes and enzymes involved in ion transport. A role in reducing the degree of ionic imbalance plays a character change in the intensity of metabolism, as well as the effect of intracellular buffer systems. Thus, increased glycolysis, coupled with the collapse of glycogen, accompanied by the release of its molecules of potassium ions, the content of which in damaged cells is lowered due to the increase of membrane permeability. Activation intracellular buffer system (carbonate, phosphate, protein) can contribute to restoring the optimum ratio in the distribution of the transmembrane and hyaloplasm ions K +, Na +, Ca2 +, etc., In particular by reducing the content of hydrogen ions in the cell. Reducing ion imbalance in turn may be accompanied by normalization of the intracellular contents and circulation of the liquid volume of cells and their organelles, and electrophysiological parameters.

Solving Problems in the genetic program of cells. Changes in the structure of DNA, leading to cell damage, can be detected and eliminated with reparative DNA synthesis enzymes. These enzymes provide the detection and removal of the modified DNA region is (they are called endonucleases or restriction enzymes), synthesis of normal nucleic acid fragment for the deleted region (by DNA polymerases) and insertion of the newly synthesized fragment to a remote location (with ligase). In addition to these complex enzyme systems of DNA repair in cells have enzymes that remove the "small-scale" biochemical changes in the genome. These include demethylase, removing methyl groups; ligase eliminating breaks in DNA strands that are caused by the action of ionizing radiation or free radicals, and others.

Compensation disorders mechanisms regulating intracellular processes. Among the responses, effectively compensating disturbances of perception mechanisms regulating cell influences include changes in the number of hormone receptors, neurotransmitters and other physiologically active substances on the surface of the cell and its organelles, as well as sensitivity (affinity) receptors to these substances. The number of receptors may vary, in particular due to the fact that their molecules can be immersed in the cell membrane, or cytoplasm and rise to the surface thereof. From the number and sensitivity of receptors, which receive regulatory incentives are largely dependent nature and severity of the response to them.

The excess or deficiency of neurotransmitters and hormones, as well as significant variations in their activity level may be so-called second implementation nerve stimulus mediators, in particular of cyclic nucleotides. It is known, for example, that the ratio of cAMP and cGMP is changed not only as a result of regulatory extracellular stimuli, intracellular factors but also, in particular phosphodiesterase, and calcium ions. Violation of regulatory effects on the implementation of the cell can be compensated to some extent on the level of intracellular metabolic processes, since many of them on the basis of flow rate regulation of metabolism amount of the enzyme reaction product (the principle of positive or negative feedback).

Reducing the functional activity of the cells. The importance among the adaptive mechanisms of damaged cells is controlled, controlled reduction of their functional activity. This causes a decrease in consumption of ATP energy substrate metabolism and oxygen needed to implement the functions and provide plastic processes. As a result, the degree and extent of damage to the cells by the action of pathogenic factors are significantly reduced, and after its termination is marked more intensive and complete recovery of cellular structures and their functions. Among the main mechanisms that explain the temporary lowering of cell function, may include a decrease in effector (incentive function) impulses from the nerve centers, reduction in the number or sensitivity to cell surface receptors, intracellular regulatory suppression of metabolic reactions, the repression of the activity of individual genes.

Adapting cells under injury occurs not only on metabolic and functional level. Prolonged repeated or serious damage causes substantial structural changes in the cell that have adaptive value. They are achieved through the processes of regeneration, hypertrophy, hyperplasia.

Regeneration (from the Latin regeneratio -. Regeneration, restoration). It means cell compensation and (or) their structural elements instead of dead, damaged, or have completed their life cycle. Regeneration structures is accompanied by the restoration of their functions. There are so-called cellular and intracellular (subcellular) forms of regeneration. The first is characterized by the multiplication of cells through mitosis or amitosis. Intracellular Regeneration manifested by reduction of organelles: the mitochondria, nucleus, endoplasmic reticulum and other instead of damaged or dead.

Hypertrophy (from the Greek hyper -. Excessively, increasing + Greek trophe -. Food). It represents an increase in an organ or part due to an increase of volume and mass of the structural elements, in particular cells. Hypertrophy of the intact cell organelles compensates breach or failure the functions of its corrupt elements. For example, tissue cell hypertrophy mitochondria undergoing repeated influence of moderate hypoxia, can provide adequate intracellular energy process even in conditions of reduced oxygen delivery and significantly reduce or prevent damage.

Hyperplasia (from the Greek hyper -.. Overly + Greek plasis - formation, formation). Characterized by increasing the number of structural elements, in particular in cell organelles. Often in the same cell and there are signs of hyperplasia and hypertrophy. Both processes provide not only compensation for a structural defect, but also the possibility of increased cell functioning.

Intercellular (system) cell adaptation mechanisms when they are damaged. Within tissues and organs are not separated cells. They interact with each other by exchanging metabolites, physiologically active substances, ions. In turn, the interaction of the body in general, cells and organs functioning ensured lymph and circulatory systems, immunobiological surveillance, endocrine and nervous influences.

Thus, a decrease in the oxygen content in the blood (which causes or can cause damage to cells, especially the brain) through reflex irritation chemoreceptors stimulate the neurons of the respiratory center. This increases the volume and alveolar ventilation eliminates or reduces the extent of lack of oxygen in blood and tissues. Damage to the cell under conditions of hypoglycemia can be reduced by increasing the production of hormones that increase in blood glucose level and its transport into cells: adrenalin, glucocorticoids, growth hormone, and others.

An example of an adaptive response such as circulatory can be increased inflow of blood through the collateral (bypass) vessels at the closing of the lumen of the main artery of an organ or tissue.

Immune mechanisms of supervision and protection are included under the influence of pathogen antigen nature. System involving immunocompetent phagocytes, and antibodies (or) inactivates T lymphocytes endo - and exogenous antigens that can damage the cells of an organism. Normally, the above and other systems provide adequate response of the whole organism to various influences endo - and of exogenous origin. In pathology, they are involved in the regulation and implementation mechanisms for the protection, compensation and rehabilitation of damaged structures and functions of cells and damaged tissues.

A characteristic feature of the intracellular mechanisms of adaptation is that they are implemented mainly with the participation of cells that have not been directly exposed to the pathogenic factor (eg, hyperthyroidism cardiomyocyte necrosis outside the zone of myocardial infarction).

In terms of implementation at the intercellular cell damage response adaptation can be divided into organ-tissue, intra, inter-system.

An example of the reaction of organ and tissue levels may be activation of the function of damaged cells of the liver or the kidney is damaged part of the body cells. This reduces the load on the cell, subjected to pathogenic effects, reduces the degree of alteration and implementation of reparative processes.

Among intra-arteriolar narrowing relates reactions with a decrease of the heart (e.g. myocardial infarction), which maintains a high level of tissue perfusion pressure and prevents (or reduces power) of cell damage.

Involvement in adaptive responses observed in several physiological systems, such as general hypoxia. This activates the breathing work systems, circulation of blood and tissue metabolism, which reduces the lack of oxygen and metabolic substrates to the tissues, increasing their utilization and thereby reduces the degree of cell damage.

Activation of intracellular and intercellular mechanisms of adaptation in case of damage, usually prevents cell death, ensures that their functions and contributes to the elimination of the consequences of the action of pathogenic factors. In this case we speak of reversible changes in the cells. If the power is high pathogenic agent and (or) the protective and adaptive mechanisms are not sufficient, develop irreversible damage to the cells and they die.