The idea of ​​a "hormone" was not well received by the scientific community and was a difficult concept to describe, as scientists were not familiar with the idea of chemical substance messengers that influence the actions of cells in the body. Many scientists, such as Arnold Adolph Berthold, Thomas Addison, Joseph von Mering and Oskar Minkowski, George Murray, George Oliver and Edward Albert Schäfer conducted experiments, studying the role of endocrine glands and their chemical messengers. However, their fellow scientists believed that the nervous system was responsible for the results of their experiments and not the chemical messengers (hormones) in the endocrine system. It was not until 1902, when two scientists, William Bayliss and Ernest Starling, demonstrated the mechanism of the hormone secretin and its ability to cause the secretion of bicarbonate in the form of pancreatic juice from the pancreas and into the duodenum during digestion. Following this discovery, endocrinology was recognized as an official branch of science, and these infamous chemical messengers that so many scientists attempted to corroborate were finally defined as hormones. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original EssayA hormone is now understood as a chemical messenger, released in very small quantities by a cell, that exerts a biological action on a target cell. A well-recognized hormone today is erythropoietin (EPO). In 1906, Paul Carnot and Clotilde-Camille Deflandre proposed the existence of a “humoral factor” that regulates erythropoiesis after noticing an increase in red blood cells in rabbits after injecting them with anemic blood. Decades later, KR Reissman and Allan Erslev elaborated on Carnot and Deflandre's findings and improved their experiment, further convincing the scientific community of the existence of a chemical messenger that plays a crucial role in erythropoiesis. In 1977, Eugene Goldwasser and his team purified and isolated this chemical messenger. Over the years scientists studied this factor, it was called hematopoietin, erythropoietic stimulating factor, etc., until it was finally accepted as "erythropoietin" (American Society of Hematology). EPO is a glycoprotein of 165 amino acids with two disulfide bonds, which is produced mainly in the kidneys and, to a lesser extent, in the liver. The exception to this occurs before birth and in those with loss of kidney function. In both of these cases, the main site of EPO synthesis is the liver. In the kidney, erythropoietin is synthesized by peritubular fibroblasts in the renal cortex. Secretion of EPO by peritubular fibroblasts stimulates erythropoiesis (red blood cell production) in the bone marrow. EPO production depends on oxygen levels in the tissues: lower oxygen levels increase EPO production and secretion, and high oxygen levels decrease EPO production and secretion. EPO has several goals and functions in the body. EPO has its effects on erythroid cells, non-erythroid cells, and non-erythroid tissue/organ systems. Specifically, EPO works in the bone marrow, which causes athletes to abuse its effects, in neurological development, in heart tissue, in the intestine, in angiogenesis, and it works to improve obesity. As already mentioned, EPO stimulates erythropoiesis in the bone marrow. This occurs in response to a low hematocrit, or the ratio of red blood cells in the blood to the total amount of blood in the body. Low levels of red blood cells in the blood mean low levels of oxygen in the blood, as red blood cells carry oxygen through the bloodstream. Low oxygen levels intissues may be the result of the body's need to replace red blood cells (due to a lifespan of 120 days), a shortened lifespan of red blood cells, blood loss, low production of red blood cells or diseases such as anemia (low level of oxygen in the tissues). levels of blood cells or hemoglobin in the blood). The kidneys are stimulated to release EPO in response to the hypoxia-inducible transcription factor complex, which regulates EPO release. This factor is highly expressed under low oxygen conditions and minimally expressed under high oxygen conditions. When the hypoxia-inducible transcription factor complex is expressed, EPO is released from the kidney and causes differentiation of erythroid progenitors in the bone marrow by binding to the EPO receptor on these cells. This causes an increase in hematocrit and, therefore, an increase in the oxygen-carrying capacity of the blood. Due to the fact that EPO increases the levels of red blood cells in the blood and, therefore, increases the oxygen carrying capacity of the blood, EPO has been highly sought after by athletes with the aim of engaging in “doping blood". Blood doping occurs when athletes take synthetic EPO to improve their performance, as they will have a greater capacity for oxygen in their bloodstream. However, many athletes don't realize that taking high doses of EPO causes oxidative stress, which results in an abundance of oxygen free radicals in the body, flooding the antioxidants in the body with more free radicals than they can handle. remove. Free radicals have a negative effect on the body's cells, destroying many crucial organelles and cellular components. Therefore, EPO doping has been banned in professional sports. Regardless, many athletes today, professional and non-professional, use EPO to improve their athletic abilities. EPO also plays a role in neurological development. Specifically, when EPO is released from the kidney, it has a direct effect on neuroblastoma cells, causing them to differentiate, and on oligodendrocytes, increasing their number. This fact manifested itself in a study conducted on children with cerebral palsy. Specifically, synthetic EPO has been shown to have healing effects on newborns, acting as a neuroprotective factor. Another study with subjects who had had an acute stroke produced the same result. Administration of EPO to these subjects has been shown to reduce stroke symptoms and improve their overall condition. Furthermore, the lack of EPO receptors in animal models, such as mice, resulted in decreased neural progenitor cells and apoptosis activity in the nervous system, indicating that EPO is necessary for proper neural function and maintenance. Furthermore, in studies conducted in vivo, EPO has been shown to function as a neuroprotective factor, protecting against brain injury. Additionally, EPO helps heart function. In an in vivo study conducted on rats with myocardial infarction, EPO administration significantly reduced cardiomyocyte apoptosis, strengthening cardiac function and increasing cardiac lifespan. EPO increases the probability of survival of endothelial cells against possible ischemic damage to the vessels of the heart, also preventing apoptosis (Bunn 2013). Similarly, in humans who have had a myocardial infarction, EPO has been shown to have healing properties, as it stimulates the formation of new capillaries in the heart. In fact, recombinant human EPO (rhEPO) has been used to reduce the size of an infarct and, in the process, promote restructuring of the left ventricle. Furthermore, EPO is.