Cell Damage – Classification, Manifestations, Mechanism, Pathogenesis

Damage is a typical pathological process, manifested by a violation of the structural and functional organization of a living system, caused by various reasons. Physiological damage is caused by the processes of natural decay and cell regeneration (with aging, prolonged inactivity).

Damage can be:

  1. reversible and irreversible;
  2. acute and chronic.

Acute damage is manifested by pre-depressive hyperactivity (increased function of organelles, primarily mitochondria, and increased production of ATP), partial necrosis (destruction of the damaged part of the cell by phagocytes) and total damage (“agony” and cell death).

“Agony” of a cell is the phase of damage, when a minimum gradient of electrolyte concentration between the cell and the extracellular environment is still maintained. When it disappears, cell death occurs .

By the ability to divide, they are distinguished:

Category I cells – by the time of birth, highly specialized, incapable of reproduction (for example, neurons of the cerebral cortex);

Category II cells are highly specialized, not capable of division, but the body has a mechanism for their continuous reproduction (for example, intestinal epithelial cells);

Category III cells – have a long life span, retaining the ability to divide (for example, hepatocytes).


1st type – damage to chromosomes: delay of cells in prophase, violation of spiralization and despiralization of chromosomes; fragmentation of chromosomes; the formation of bridges between chromosomes in anaphase; early separation of sister chromatids; damage to the kinetochore.

Type 2 – damage to the mitotic apparatus: delay in the development of mitosis in the metaphase; dispersal of chromosomes in metaphase; group metaphase; multipolar mitoses; asymmetric mitoses; monocentric mitoses; K-mitosis.

3rd type – violation of cytotomy: premature cytotomy; delayed cytotomy; lack of cytotomy.

Non-specific manifestations of cell damage:

violation of the disequilibrium state between the cell and the external environment;

violation of the structure and function of membranes:

  1. membrane transport,
  2. membrane permeability,
  3. changing the communication of cells and their “recognition”,
  4. changes in membrane mobility and cell shape (exotropia, esotropia, simplification of the cell surface),
  5. changes in the synthesis and exchange of membranes;
    • damage potential (membrane potential) – the potential difference between the damaged and undamaged cell surface;
    • violation of water exchange;
    • violation of electrical conductivity (tissue impedance);
    • violation of the activity of the enzyme systems of the cell (up to the autolysis of the cell);
    • decrease in oxidative phosphorylation;
    • reduction of redox potential;
    • damage acidosis (primary and secondary);
    • changes in the sorption properties of the cell.

Labilizatory lysosomal membranes – endotoxins and mycotoxins bacteria, carcinogens, phospholipases, activators of lipid peroxidation (LPO), hypoxia, shock, etc.

Lysosomal membrane stabilizers – anti-inflammatory hormones, cholesterol, chloroxin, etc.

Lysosomal diseases (diseases of “storage”, or thesaurismosis ) are manifested by a defect (absence) of one or more lysosomal enzymes, which leads to the accumulation in the cell of substances that are normally metabolized by this enzyme (for example, hepatosis, glycogenosis, etc.).

Physiological regeneration is the replacement of worn-out structures with new ones during life.

Reparative regeneration is the restoration of a certain volume of dead tissue. May be complete or incomplete.

Mechanisms of long-term adaptation of a cell to a pathogenic factor (according to FZ Meerson ).

  1. Mobilization of a functional system specifically responsible for adaptation to this specific factor.
  2. Non-specific activation of stress-realizing systems.
  3. Conjugated enhancement of the physiological function and genetic apparatus of the cell: enhancement of the synthesis of nucleic acids and proteins that form key cell structures.
  4. Formation of a systemic structural trace of adaptation.

The phenomenon of adaptive stabilization of structures (FASS) is manifested by an increased resistance of cellular structures to damage in previously adapted organisms. An important role in the development of FASS is played by the so-called stress proteins (“heat shock proteins”), which prevent denaturation of membrane proteins. Reduced glutathione, natural structural antioxidants such as vitamin E and cholesterol are also referred to as cellular defense systems.