CHARACTERISTICS TYPICAL FORMS OF CELL DAMAGE

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Damage to cells is characterized by the development of a variety of complex changes in them. However, they can be grouped into several groups.

The main groups of typical forms of cell damage

1. Dystrophy.

2. Dysplasia.

3. Typical violations of subcellular structures and components.

4. Necrosis

Dystrophy

Under dystrophies (from the Latin dys -. Breach + Greek trophe - I feed) understand the metabolism in the cells, accompanied by disturbances of their functions, processes and plastic structural changes, leading to disruption of their livelihoods.

The main mechanisms dystrophies are:

- The synthesis of abnormal substances in the cell, such as protein-polysaccharide complex amyloid;

- Excessive transformation of some compounds in others, such as fats and carbohydrates into proteins, carbohydrates into fat;

- Decomposition (Phanerozoic), for example, protein-lipid membrane complexes;

- Infiltration of the cells (intercellular substance and) organic and inorganic compounds such as cholesterol and its esters arterial wall in atherosclerosis.

The main cell types of dystrophies, depending on the species mainly disturbed metabolism include: 1) protein (disproteinos); 2) fat (lipidoses); 3) carbohydrate; 4) pigment; 5) mineral.

1. Disproteinos. They are characterized by a change in physico-chemical properties of proteins, cells, and as a consequence of a violation of their enzymatic and structural functions. Most often disproteinozy appear as granular, hyaline droplet and hydropic dystrophy. Often they represent successive stages metabolic disorders cytoplasmic proteins, leading to cell death.

When granular dystrophy appear in the cytoplasm granules (grains) protein. They are formed as a result of infiltration (penetration) it from the interstitial fluid, the transformation of carbohydrates and fats in the proteins decay (decomposition) and lipoprotein cytoplasmic membrane. One of the main reasons for the general granular dystrophy is a violation of the energy cells.

Hyaline degeneration is characterized by the accumulation of the protein in the cytoplasm of acidophilic mostly hyaline inclusions ("drops"). Simultaneously revealed signs of degradation of cellular organelles. Signs of hyaline degeneration observed in conditions that increase the permeability of cell membranes.

Hydropic (hydropic, vacuolar) degeneration is the result of such changes in the physicochemical properties of cytoplasmic proteins, which is accompanied by an increase in oncotic pressure cell hydration and excess protein micelles. The cytoplasm of cells formed vacuoles filled with liquid and containing no lipid or glycogen. Electron microscopy shows signs of intracellular organelle swelling and edema. The most common causes are hydropic dystrophy hypoxia, exposure to ionizing radiation, toxins, microbes and parasites, malnutrition.

2. Lipidosis. To include various lipids on the chemical composition of substance, insoluble in water.

Lipidoses manifested either by increasing intracellular lipid content, or the appearance of cells, where they are normally absent or abnormal formation of the chemical composition of lipids.

Lipidoses, as well as disproteinozy most frequently observed in the cells of the heart, liver, kidney, brain and have corresponding names (fatty degeneration of the heart, liver, kidney, brain).

3. Carbohydrate dystrophy. Characterized by impaired metabolism of polysaccharides (glycogen, mucopolysaccharides) and glycoproteins (mucin mucoids).

"Polysaccharide" dystrophy appear:

1) reduction of their content in the cell (e.g., glycogen diabetes); 2) the lack of, or a significant reduction (aglikogenozy) or 3) the accumulation of excess (glycogen infiltration cells glycogenoses).

The reason carbohydrate dystrophies are often endocrinopathies (eg, insulin deficiency), or fermentopathy (no or low activity of enzymes involved in carbohydrate synthesis and decay processes).

Carbohydrate dystrophy, metabolic disorders related glycoproteins are characterized as typically accumulation and mucins mucoids with mucous consistency. In this regard, they are called mucous dystrophies. The reasons most often serve their endocrine disorders (eg, insufficient production, or low activity of the thyroid gland hormones) as well as direct damaging effects on the cells of pathogenic factors.

4. Pigment dystrophy (dispigmentos). Pigments of the human body and animal cells are involved in the implementation of many functions: synthesis and catabolism substances, reception of various influences, protection from damaging factors.

Cell pigments are hromoproteidov, ie compounds composed of protein and dye.

Depending on the biochemical structure of the endogenous cellular pigments separated as follows: 1) gemoglobinogennye (ferritin, hemosiderin, bilirubin, hematoidin, hematin, porphyrin); 2) proteinogenic, tirozinogennye (melanin adrenochrome, pigments ochronosis and enterochromaffin cells); 3) lipidogennye, lipoproteinogennye (lipofuscin, gemofustsin, ceroid, lipochromes).

All dispigmentozy are divided into several groups depending on their origin, development mechanism, the biochemical structure of the pigment, manifestations and prevalence.

Types dispigmentosis

I. By origin:

- Primary (hereditary, congenital).

- Secondary acquired (occurring under the action of pathogenic agents during postnatal life of the organism).

II. On the mechanism of development:

- Caused by defects in enzymes (fermentopathy) pigment metabolism and (or) changes in their activity.

- Related to the changes in the content and (or) activity of transport enzymes, pigments across the cell membrane.

- Cause damage to cell membranes.

- Caused by an excess accumulation of pigments in the cells which have the property of phagocytosis.

III. According to biochemical structure of the pigment:

- Hemoglobinogenic "iron dependent".

- Proteinogenic, tirosinogenic.

- Lipidogenic, lipoproteinogenic.

IV. As manifestations:

- The appearance of pigment cell that is not in its normal.

- Accumulation of excess pigment formed in the cell as normal.

- Reducing the amount of pigment formed in the cell as normal.

V. By the prevalence of:

- Local (regional).

- General (common).

Hemoglobinogenic dispigmentosis include hemosiderosis, hemochromatosis, hemomelanosis, porphyria, excess accumulation of direct bilirubin in the hepatocytes.

Most hemoglobinogenic pigments are products of hemoglobin catabolism. Some (ferritin, hemosiderin) are formed with iron absorbed from the intestine.

Part hemoglobinogenic dispigmentosis is the result fermentopathia. These include, in particular, primary hemochromatosis and porphyria.

Primary Hemochromatosis - a disease caused by a genetic defect (transmitted by autosomal dominant) of enzymes involved in the processes of iron transport from the gut cavity. In this case, the blood enters the excess iron that accumulates in the form of ferritin and hemosiderin in the cells of various tissues and organs (liver, myocardium, skin, endocrine glands, salivary glands, and others.). Similar changes are also observed in secondary hemochromatosis. It is the result or acquired deficiency of enzymes that ensure the exchange of dietary iron (alcoholism, intoxication), or - high iron organism revenues from iron-containing foods or drugs, or a consequence of excessive red blood cell hemolysis.

Porphyria is characterized by the accumulation in the cells uroporphyrinogen I, porfobilina, porfirinogenov. One of the common causes of porphyria is the lack of or low kinetic activity of enzymes of porphyrin metabolism (eg, uroporphyrinogen-W-kosintetazy) hereditary or acquired nature.

Most other species hemoglobinogenic dispigmentosis (hemosiderosis, hemomelanosis) are the result of excessive accumulation of pigments in the cells due to increased hemolysis of red blood cells of various origins (for infections, intoxications, inogrupp transfusion of blood, Rh-conflict, and others.).

Proteinogenic (tirosinogenic) dispigmentosis manifest enhancement or suppression of pigmentation of tissues (local or general) products of tyrosine metabolism.

Increased pigmentation is often the result of excess melanin in the cells (melasma, from the Greek, melas - dark, black). Observed in adrenal insufficiency caused by a decrease in their weight, for example when they are tuberculous or neoplastic lesions; a pituitary adenoma, hyperthyroidism, ovarian tumors. It is believed that an excess of melanin in the cells is a result of its increased synthesis of tyrosine instead of adrenaline. Process melanin formation potentiated ACTH level is elevated in a shortage of adrenaline in the blood.

Accumulation of pigment ochronosis (from the Greek ochros -. yellow, yellow) in cells is observed in the primary (hereditary) fermentopathy characterized by deficiency of enzymes of metabolism of phenylalanine and tyrosine. This hyperpigmentation is local or widespread in nature. The pigment accumulates in the cells of the tissues of the nose, ears, sclera, trachea, bronchi, tendons, cartilage, etc.

Attenuation tissue pigmentation, or lack of pigment in their cells (albinism, lat albus -. White) may also be a primary or secondary origin. In albinism Melania absent from the skin cells of the iris eye, hair. The reason for this is most often a hereditary lack of the enzyme tyrosinase in cells. In the case of a local reduction of pigmentation, such as the skin (leukoderma, vitiligo) is essential secondary violation exchange of melanin due to neuroendocrine disorders of its regulation (at hypoinsulinism, reducing the level of parathyroid hormone), due to the formation of antibodies to melanin or as a result of increased destruction of melanocytes in inflammation or tissue necrosis.

Lipidogenic dispigmentosis characterized most often increase the amount of pigment in the cells of the lipid and lipoprotein nature (lipofuscin, hemofuscina, lipochromes, ceroid). All these pigments are very similar on basic physical and biochemical properties. In humans, usually there are various options for local lipofuscinosis hereditary (rarely) or acquired (usually) origin.

It is believed that the main causes are acquired lipofuscinosis tissue hypoxia, a deficiency in the body of vitamins, protein and certain types of lipids. Lipofuscinosis most commonly develops in middle and old age people on chronic "metabolic" disorders.

Hereditary and congenital lipofuscinosis characterized by excess accumulation of lipofuscin in the cells, usually combined with fermentopathy (ie these are an option lipofuscinosis storage diseases). Examples of these diseases may be neuronal lipofuscinosis (excess deposition of lipofuscin in neurons, combined with a decrease in intelligence, vision, hearing, development of seizures); lipofuscinosis liver, combined with bilirubin metabolism disorders caused by inherited defects of enzymes and transport glucoronisation bile pigments.

5. Mineral dystrophy. Shows a significant decrease or increase in the mineral content in the cells. The most important are violations of exchange of calcium compounds, potassium, iron, zinc, copper. Their ionized fraction and molecular processes involved in the regulation of cell membrane permeability, enzyme activity, and the formation of peace-building activities, the implementation of the action of hormones and neurotransmitters, the electromechanical coupling in myocytes and many others.

Mineral dystrophy characterized by the accumulation of excess in the cells of the molecular or ionized cations fractions (such as calcifications, siderosis, deposition of copper at hepatocelebral dystrophy) or a decrease in their content.

One of the most common species in the human cell is a mineral dystrophies calcification - accumulation ("deposition") of excess calcium in the cells. Calcification may be general or local. On the "territory" of the cell to the greatest extent calcium salts accumulate in mitochondria, lysosomes (phagolysosomes) in the tubules of the sarcoplasmic reticulum. The main reason is to change cellular calcification physicochemical properties hyaloplasm cell (e.g., intracellular alkalosis), combined with calcium absorption. The most frequently observed calcification of myocardial cells, renal tubular epithelium, lung, gastric mucosa, the walls of arteries.

Among dystrophy refers also thesaurismosis (from the Greek thesauriso - accumulation, absorption, float). They are characterized by an excess accumulation of various substances in the cells, which is accompanied by breach of their structure and function, and - the intensity and nature of the plastic and metabolic processes in them.

Almost all tesaurismosis - the result of a hereditary pathology of enzymes, transmitted, as a rule, an autosomal recessive manner. Inheritable change in the genetic program are responsible for a defect of enzymes (lysosomal, membrane-free). The result is a metabolic disorder in the cell that makes the accumulation of excess in it products of incomplete or abnormal cleavage of substrates.

Depending on the structures of biochemical substances accumulate in the cells tesaurismosis separated into lipid (lipidoses), glycogen (glycogenoses), amino acid, nucleoprotein, mucopolysaccharide, mucolipid. The most common varieties are tesaurismosis lipid and glycogen.

Dysplasia

Dysplasia (from dys - disorder disorder Greek plasis + -. The image) - the common name of disturbances of development (differentiation, specialization) of cells exhibiting persistent changes in their structure and function, which leads to the breakdown of their life.

The causes of dysplasia are factors of physical, chemical or biological nature, damaging the genome of the cell. In this case it violated the genetic program of cells or the mechanisms of its implementation. That is what makes resistant and, as a rule, inherited from cell to cell changes unlike dystrophies, which often are temporary, reversible and can be eliminated at the termination of the causal factor.

The main mechanism of dysplasia is a disorder of the differentiation process, which is to form the structural and functional specialization of cells. Cellular differentiation is mainly determined by genetic program. However, the implementation of the program to a large extent depends on the complex interactions of the nucleus and the cytoplasm, the cell microenvironment, influence on it of biologically active substances and many other factors. That is why even if the same change in the genome of different manifestations of dysplasia cells can be different character.

Dysplasia manifest changes in the size and shape of cells, their nuclei and other organelles, the number and structure of chromosomes. Typically, cells are increased in size, have irregular, bizarre shape ("monster cells"), the ratio of different organelles in them disproportionately. Often in such cells are found various inclusions, symptoms of degenerative processes.

Examples of cellular dysplasia can be called education megaloblasts in the bone marrow with pernicious anemia, sickle-shaped red blood cells in the presence of abnormal hemoglobin, the major neyronov- "monsters" in the defeat of the cerebral cortex (tuberous sclerosis), polynuclear giant cells with bizarre arrangement of chromatin in neurofibromatosis (illness Recklinghausen). Cellular dysplasia is one of the manifestations of atypism tumor cells.

Necrosis and autolysis. Apoptosis

Damage to individual components of the cell affects the state of all its structures and processes, as they are combined into a single balanced system that is included in turn in tissue cells ensemble. This integration allows you to eliminate the consequences of damage in a single cell, if it is the strength and severity of the relatively small (reversible injury). If the interaction of subcellular structures and coordination process under the influence of intracellular pathogen violated, broken and homeostasis of cells, it dies - necrotic or undergoes apoptosis (permanent damage).

Necrosis (from the Greek Necros -. Dead) - cell death, accompanied by the irreversible cessation of their activity. Necrosis is often the final stage of dystrophy, dysplasia, as well as a consequence of the direct action of damaging factors of considerable strength. Changes prior to necrosis or necrobiosis called patobiozom.

Most of the dead cells are subjected to autolysis, ie self-destructive patterns. The main mechanism of autolysis is the hydrolysis of components of cells and intercellular substance under the influence of lysosomal enzymes. This contributes to the development of acidosis in damaged cells. During autolysis participate as free radicals. One of the arguments is the fact lipoperoksidnyh intensification of free radical reactions and tissue damage in inflammation, at certain stages of infarction, tumor growth and other pathological processes.

During lysis of damaged cells may participate and other cells - phagocytes and microbes. In this connection, as opposed to the last mechanism called autolytic heterolytic.

Thus lysis of necrotic cells (necrolysis) may be provided auto- and heterolytic processes in which enzymes are involved and other factors such as the dead and contacting them with living cells.

Apoptosis (from the Greek apo -. The absence, denial of something, ptosis - falling) - the genetically programmed process of termination of life and death of cells or groups of cells in a living organism. Thus, the dead cells is not exposed to autolysis, and typically is absorbed and degraded phagocyte. The process of apoptosis observed in the pathological tissue wasting, inflammation, tumor growth; its frequency increases with aging.

Manifestations of damaged cells

Any damage causes cells in her complex specific and nonspecific changes, detectable by various methods: biochemical, physico-chemical, morphological and others.
Under the specific properties of the cells to understand the changes that are typical of this factor under the action of its various cells or characteristic only this type of cells when exposed to damaging agents of various kinds. Thus, an increase in any cell osmotic pressure, accompanied by her overhydration, stretching membrane, a violation of their integrity. Influenced releasers process of oxidation and phosphorylation is reduced or blocked by pairing these processes and decreases the effectiveness of biological oxidation. The high concentration in the blood of one of adrenocortical hormones - aldosterone - causes accumulation of different cells in excess of sodium ions. On the other hand, the effect of damaging agents to specific cell types is specific to them (cells) changes. For example, the impact of the various (chemical, physical, biological) of pathogenic factors on muscle cells accompanied by the development of contracture of myofibrils, neurons - the formation of the so-called potential damage to the red blood cells - hemolysis and their exit from their hemoglobin.

Damage to the cells is always accompanied by a complex and non-specific, stereotypical, standard changes in them. They are identified in the various cell types of the action of various agents. Among the frequent non-specific manifestations of alterations in the cells are acidosis, excessive activation of free radical and peroxide reactions, denaturation of the protein molecules, increased permeability of cell membranes, ion imbalance and fluid, changing the parameters of the membrane potential, increase the sorption properties of the cells.

Detection of the complex specific and nonspecific changes in the cells of organs and tissues makes it possible to judge the nature and potency of the pathogenic factors, on the extent of damage, as well as on the effectiveness used for the treatment of drug and non-drug means. For example, to change the activity in the blood plasma of specific cell myocarditis MB-isoenzyme of creatine kinase, and the content of myoglobin in comparison with the level of potassium ions dynamics (emerging from the damaged cardiocytes), ECG changes, indicators of contractile function of different parts of the myocardium can be judged on the degree and extent of damage heart when a heart attack.