Thromboxane is one of the prostaglandins and is responsible for platelet aggregation. It is found only in platelets. A permanently too high concentration of thromboxane leads to arteriosclerosis and cardiovascular disease in the long term.
What is thromboxane?
Thromboxane is named after platelets because it is found only there. It is responsible for platelet aggregation. In the body, it is formed from arachidonic acid. Arachidonic acid is an omega-6 fatty acid with four double bonds. During thromboxane synthesis, this forms a so-called oxane ring consisting of five carbon atoms and one oxygen atom. With the help of the enzymes cyclooxygenase and peroxidase, prostaglandin H2 is formed first. Prostaglandin H2 is a peroxide, which is immediately converted into prostaglandin A2 by thromboxane synthase. Prostaglandin A2 has an oxygen bridge over the oxane ring, so this compound is very active and has a half-life of only about 30 seconds. During this time, the hormone mediates its effect and is converted to the inactive form prostaglandin B2. Thromboxane is a tissue hormone and acts only locally. The starting compound arachidonic acid is obtained from the phospholipids of the cell membrane before thromboxane synthesis. With the help of phospholipase A2, it is cleaved from the membrane lipids. In addition to thromboxane, arachidonic acid also forms a variety of prostaglandins, which mainly exhibit proinflammatory effects.
Function, effects, and roles
The main function of thromboxane is platelet aggregation to form thrombi for wound closure and to stop bleeding. Thromboxane is formed only in platelets. Platelet formation is a complicated hormonally triggered process that occurs mainly in injuries and open wounds. In order to stop the bleeding quickly, several processes take place. Shortly after the bleeding occurs, contraction of the blood vessel at the injured site takes place. Already the vasoconstriction is mediated by thromboxane via a G-protein. Afterwards, the blood circulation decreases at first. Supported by the reduced blood circulation, the second step can take place. Platelets undergo adhesion and activation. Adhesion is mediated by certain glycoproteins. Activation via glycoprotein receptor IIb/IIIa initiates the signal for platelet aggregation. In this process, the platelets change their shape. Together with thrombin and ADP, thromboxane now ensures platelet aggregation. Initially, aggregation is reversible. However, when a certain concentration of the release products is reached, this process becomes irreversible. After that, a network of fibrin is formed so that the injured site closes permanently. Thromboxane has a strong antagonist. This antagonist is prostacyclin, which is also a prostaglandin derived from arachidonic acid. Prostacyclin initially counteracts vasoconstriction and thus indirectly impedes thrombus aggregation. Finally, it also directly prevents platelet aggregation. This regulatory mechanism is important for achieving a balanced relationship between blood clotting and blood flow. Because even the smallest injuries can otherwise become the starting point for the development of thrombosis.
Formation, occurrence, properties, and optimal values
Thromboxane is just one prostaglandin that is formed from arachidonic acid. Yet arachidonic acid is one of the major precursors for several proinflammatory prostaglandins, all of which have the same basic structure. They consist of the scaffold of prostanoic acid. Arachidonic acid is absorbed through food. Particularly high amounts of arachidonic acid are found in animal fats, although it is an unsaturated fatty acid with four double bonds. However, it is also synthesized in the organism from the essential omega-6 fatty acid linoleic acid. In this process, arachidonic acid is formed via the intermediate stages gamma-linolenic acid and dihomogammalinolenic acid. Linoleic acid is abundant in vegetable oils. However, the synthesis of arachidonic acid from linoleic acid is not very productive, so it is considered a semi-essential omega-6 fatty acid.
Diseases and disorders
As mentioned earlier, the prostaglandins in arachidonic acid are particularly pro-inflammatory and also promote blood clotting via thromboxane.These processes are very important for the body and represent reactions of the immune system to infections, injuries and other external influences. At the same time, prostaglandins from arachidonic acid also irritate pain receptors, causing severe pain. There are counterpart prostaglandins formed from dihomogammalinolenic acid or alpha-linolenic acid. These have anti-inflammatory and anticoagulant effects. However, prostacyclin from the arachidonic series is also anticoagulant, but also strongly proinflammatory. It plays a special role in connection with allergies and asthma. The sometimes very strong opposing effects of the prostaglandins require a balanced relationship between the active substances. This already starts with the diet. For example, the ratio of omega-6 and omega-3 fatty acids is of great importance for health. This ratio should be 6 to 1. If the intake of omega-3 fatty acids is too low, prostaglandins, which promote inflammation and blood clotting, will predominate. In the long term, this can lead to arteriosclerosis, cardiovascular disease, thrombosis, allergies, asthma or rheumatic complaints. If the concentration of thromboxane in the body is elevated for a long time, there is a risk of increased thrombosis. The smallest injuries to the blood vessels always occur. However, these could be the starting point for constant platelet aggregation. On the one hand, thromboses can develop, and on the other hand, in connection with inflammatory processes, deposits can gradually form in the blood vessels in the form of plaques. The result is arteriosclerosis with the risk of heart attacks, pulmonary embolisms and strokes. It is also known that poor diet, alcohol and cigarette abuse, too little exercise, obesity, diabetes mellitus and various diseases have an unfavorable effect on the ratio of unsaturated fatty acids in the body in favor of arachidonic acid. This increases the risk of arteriosclerosis and thrombosis.
