Lysosomes are cytoplasmic granules which contain a variety of potent hydrolytic enzymes bound in a latent form in a relatively impermeable membrane. These enzymes are capable of hydrolyzing a wide variety of both natural and synthetic substances and can digest all intra-and extracellular macromolecules if they are released from their membranes. When released from the organelles, either inside or outside the cell, as a consequence of certain forms of cellular injury, they may contribute to the pathogenesis or the propagation and perpetuation of shock. They are most active at an acid pH, which would make them potentially more destructive in the setting of hypoxia and shock.
Numerous morphologic and biochemical observations implicate the lysosomal enzymes in the perpetuation of shock, but at this time the evidence for their primary involvement is not convincing. In organs such as liver, spleen, and intestine, thelysosomes enlarge and lose their granules dunng the early phases of shock. This is associated with a decrease in the total activity of lysosomal hydrolases in tissues and a corresponding increase in activity in the soluble fraction of the tissue homog-enate. This indicates a loss of lysosomal membrane integrity in vivo. The lysosomes obtained from animals in shock demonstrate an enhanced release of enzymes in vitro. A reduction in lysosomal membrane integrity has also been observed in animals after the administration of endotoxin. In several animal studies the levels of hydrolases found in blood, lymph, or serum seem to correlate with severity of shock.
Function of Lysosomes
Lysosomes perform various functions, the most important role is in the enzymatic digestion of various substances, both internal and external, for proper elimination.
The lysosomes can join together and form more complex organelles of structure and size.
If the primary lysosome captures an atmosphere, the cell digestion process is started. The organoid, which is able to split compounds with enzymes, already belongs to the category of secondary lysosomes. As a result of the digestion of substances, condensed residual bodies can form (this is the third phase of the lysosome life cycle).
Functions of organelles
We examined the types of lysosomes, the structure and the functions (table) – this is our next question. We decided to use the most intuitive and understandable form, that is, the table.
|Intracellular digestion||Lysosomes contain a large number of enzymes, they are able to split any compound by hydrolysis. And intracellular digestion takes place. The substances enter the lysosome and are processed by forming low molecular weight compounds, which the cell then uses for its own needs.|
|autophagy||This process allows you to get rid of useless or old organelle cells. Autophagy is a method for renewing cell organelles.|
|autolysis||In another way, this process can be called self-destruction of the cell. When the membranes of all the lysosomes of a cell are destroyed, the latter dies.|
The appearance of a myocardial depressant factor or factors (MDF) in shock, although still controversial, may be an indirect manifestation of the effect of lysosomal enzymes. In experimentally induced pancreatitis and in a variety of other shock states, plasma MDF activity closely parallels lysosomal hydrolases in the plasma. It has been suggested that pancreatic ischemia associated with shock results in the release of lysosomal and other enzymes within the pancreas, which act on an endogenous substrate to yield a peptide with low molecular weight and MDF activity, which is then released into the circulation. The resulting myocardial depression maintains the state of low cardiac output and sustains shock.
Another indication of the involvement of MDF has been the reproducibility of the shock syndrome with infusion of lysosomal hydrolases in animals. These animals demonstrate the hypotension, circulatory collapse, and pathologic changes in the tissues that are seen in experimental forms of shock.
Other suggestive evidence of the involvement of MDF has been the responsiveness of certain animals in shock to large amounts of corticosteroids. In vitro, corticosteroids stabilize the lysosomal membranes and prevent their lysis. Treatment with steroids has been shown to suppress circulating serum levels of lysosomal hydrolases in a variety of shock states.
Endotoxemia is associated with increased levels of serum hydrolases, but in vitro the endotoxins do not increase the lysis of lysosome. It has been suggested that endotoxins may cause the formation of a lysosomal releasing factor, LRF, through activation of the alternative as well as the classic complement pathways. Activation of complement in fresh human serum has been found to generate a factor (LRF) which stimulates human polymorphonuclear leukocytes to release their lysosomal enzymes. This factor has many of the properties of human C5a, a complement component known to have chemotactic and anaphylatoxin activities.