Erythrocytes or red blood cells are the most common types of cells in the blood. Because they contain hemoglobin, these cells are responsible for transporting oxygen in the blood to different types of tissues and organs in our body.
Having such an essential function, it is not surprising that there are about 5,000,000 erythrocytes per cubic millimeter of blood, which is 1,000 times more than the number of white blood cells.
These cells are very characteristic because they do not have a nucleus or mitochondria and therefore can only obtain energy through the breakdown of glucose. Their functionality is very limited, as they cannot synthesize proteins, which is why erythrocytes are considered, literally, as “bags of hemoglobin”.
Hematopoiesis is the process by which these unique cell types are synthesized. This mechanism is well known in the biological and medical fields, because it is one of the first ways to be studied due to its physiological importance. Something much less common, on the other hand, is the process by which the “pulled” red blood cells are eliminated. Today we tell you all about hemocatéresis or erectosis. Don’t miss it.
What is hemocatéresis?
From a simple physiological point of view, we can define hemocateresis as the process by which degenerating red blood cells are eliminated in the spleen and liver. These cell types have a half-life of 120 days and, as they age, are destroyed by mechanisms of cellular apoptosis.
We have introduced a striking term worth stopping in: apoptosis. We can define this physiological process as “programmed cell death”, a set of biochemical reactions that occur in multicellular living things so that the degenerated cell dies without harming the organization of the tissues to which it belongs.
The process of apoptosis is completely normal because, without going any further, the epidermal cells are in constant substitution. Studies estimate that about 3,000,000 cells die naturally in our body every second, Value that increases in the face of injury or serious infectious processes such as necrotizing fasciitis.
However, erythrocytes, red blood cells, or red blood cells (as they are called) are anything but normal cells. Therefore, we dedicate the following lines exclusively to elucidate how these aged entities end up disappearing from our bodies.
The fascinating process of eryptosis
As we said before, humans have a huge amount of red blood cells per liter of blood, as these make up 10% of the total cell volume totaling all of our tissues. Circulating erythrocytes have a half-life of 120 days, but are continuously exposed to physiologically demanding factors, such as oxidative stress in the lungs and hyperosmotic conditions when passing through the kidneys several times a day.
So there comes a time when the “life” of these cell bodies is exhausted. Like any process involving the presence of cells, their generation and replacement should be strictly regulated, which is why in many cases the very genesis of erythrocytes is considered partial apoptosis. (Since the nucleus and mitochondria are lost in their differentiation, for example). The fate of these cells has been sealed from the start.
Let’s keep it simple: As an erythrocyte ages, a number of IgG immunoglobulin-like proteins (antibodies) attach to it. The function of these antibodies is to “signal” the aged red blood cell so that the Kupffer cells in the liver can phagocytize them. The main molecular mechanisms involved which signal this “aging” of the erythrocyte are:
- The decrease in the energy load of circulating red blood cells.
- Decreased reducing power of erythrocytes.
- Presence of osmotic stress.
Some of these 3 cellular mechanisms (or all 3 at the same time) are the ones that cause the hemocateresis event, that is, the same senescence of red blood cells is phagocytosed and not reincorporated into the circulating blood.
Once swallowed …
Once these red blood cells are phagocytosed in the spleen, liver and bone marrow, hemoglobin is recycled. The “globin” part, that is to say the protein part, is recycled and broken down into amino acids which can be used for the synthesis of other molecules essential to the organism. The “heme” part; on the other hand, it is a non-protein prosthetic group, therefore it cannot be broken down into useful forms in such a simple way.
Therefore, this “heme” group dissociates into iron and bilirubin, One last molecule that may seem close to more than one drive. Bilirubin is a waste product secreted by the bile in its conjugated form, so it can be said that it ends up being released into the duodenum by the process of digestion. On the other hand, iron can be stored in the form of certain specific molecules or returned to the spinal cord, where it will again become part of new red blood cells.
But it doesn’t all end here. Bilirubin passes through the small intestine, but in the large intestine, bacterial colonies turn it into urobilinogen. Part of this compound is reabsorbed in the blood and excreted in the urine, while another part is excreted in the stool (as manure), a pigment that gives the stool that characteristic brown color.
After briefly following this path, we can see how the body is not free from all that is not completely unnecessary. Many components of dead red blood cells end up being reused, while bilirubin is released with the bile in the duodenum, which in turn is part of a digestive precursor. Of course, the perfect machinery of the human body leaves nothing to chance.
Erythosis VS apoptosis
As you can imagine, the death of a red blood cell is very different from the senescence of a cell in normal tissue. Typical events of apoptosis include nuclear condensation, DNA fragmentation, rupture of nuclear membranes, mitochondrial depolarization, and many other events that directly in red blood cells cannot occur due to the absence of these structures.
However, it should be noted that the two processes are relatively similar and the goal is common: to replace a group of cells whose useful life has ended.
Diseases associated with hemocateresis or erectosis
Hemocateresis or erectosis is not always a normal and programmed mechanism, therefore there are certain pathologies that can advance the death of red blood cells and their resulting degradation.
Malaria is a clear example. More than 400,000 people die each year from this parasite (mainly Plasmodium falciparum), which is transmitted to humans by the bite of infected mosquitoes and ends up spreading in the bloodstream and infecting red blood cells. Once inside, the pathogens multiply and cause them to rupture prematurely, which releases even more parasites into the bloodstream to infect more red blood cells.
All this causes severe physiological disturbances causing anemia, bloody stools, chills, sweating, seizures, headaches and even coma and death. Without treatment, up to 40% of those infected eventually die. This is a clear example of what happens when an unscheduled hemocateresis or erythrosis occurs en masse, and the danger that entails.
Another less aggressive but equally important example is lack of iron. A deficiency of iron in the body makes the “heme” part of hemoglobin smaller and less efficient, which is why the red blood cell has its half-life reduced. From the entry of parasites into the body to a lack of nutritional intake, the half-life or pattern of senescence of red blood cells in our body can be disturbed.
As you may have read in these lines, hemocateresis or eryptosis is a process that divides into two important phases: the signaling and phagocytosis of the senescent red blood cell and the various metabolic pathways that follow its components to. ” that they end up being reused or excreted in the urine and / or feces.
If we want you to stick with one idea of all this biochemical conglomerate, it’s like this: red blood cells are atypical cells, which is why their process of senescence is different from that of a cell found in all normal tissue.. However, the process of erectosis and apoptosis has a specific goal, the elimination of cells that have ceased to be useful to the body and replace them with new ones.
- Escorza, MAQ and Salines, JVC (2006). Eriptosis, erythrocyte apoptosis. Journal of Biochemical Education, 25 (3), 85-89.
- Herlax, V., Vazquez, R., Mate, S., and Bakas, L. (2011). Eriptosis, suicidal erythrocyte death: mechanism and associated diseases. Latin American Clinical Biochemistry Act, 45 (2), 287-296.
- Malaria, Medlineplus.gov. Collected December 25 at https://medlineplus.gov/spanish/ency/article/000621.htm#:~:text=La%20malaria%20es%20causada%20por,forma%20de%20par%C3%A1sitos%2C% 20 called% 20merzo% C3% ADtos.
- Manzur-Jattin, F., Moneriz-Pretell, C., Corrals-Santander, H., and Cantillo-García, K. (2016). Eriptosis: molecular mechanisms and their implication in atherothrombotic disease. Catalan Society of Cardiology, 23 (3), 218-226.