Catalog No.: 101297
Net Contents: 3 x 0.5 mL
ARACHIDONIC ACID Sodium Arachidonate
Arachidonic Acid Reagent Sheds Light on Thromboxane A2 Activation in Routine Plasma Studies
Arachidonic Acid (Sodium Arachidonate) Reagent is for routine use in demonstrating thromboxane A2 activation response in Platelet Rich Plasma samples.
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Stimulates Platelets to Convert COX 1 Enzyme into TX A2
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Demonstrates the Efficacy of TX A2 Platelet Activation Pathway
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Shows the Increase in Microparticles and Activated Platelets in Response to
Increasing Concentrations -
May Cause Lysis of Red Blood Cells and Subsequent ADP Dependent Platelet Activation Responses in Platelet Rich Plasma Samples
PRODUCT DETAILS
The Arachidonic Acid (Sodium Arachidonate) Reagent stands as an indispensable tool for routine investigations, specifically designed to showcase the intricate thromboxane A2 activation response within Platelet Rich Plasma samples. This multifaceted reagent operates on various fronts, unraveling key aspects of platelet behavior.
At its core, the reagent stimulates platelets, inducing a cascade of biochemical reactions that culminate in the conversion of the COX 1 enzyme into thromboxane A2 (TX A2). This enzymatic transformation serves as a pivotal point of interest, demonstrating the efficacy of the TX A2 platelet activation pathway. By doing so, it provides valuable insights into the underlying molecular processes governing platelet reactivity.
Furthermore, the Arachidonic Acid Reagent goes beyond mere stimulation, offering a comprehensive view of the platelet response spectrum. It effectively showcases the escalation in microparticles and activated platelets in direct correlation to increasing concentrations of the reagent. This dynamic observation allows researchers to discern nuanced changes in platelet behavior under varying conditions, contributing to a more profound understanding of thromboxane A2 activation.
However, this comprehensive exploration is not without its nuances. The reagent's interaction with Platelet Rich Plasma samples may induce the lysis of red blood cells, setting the stage for subsequent ADP-dependent platelet activation responses. This phenomenon adds a layer of complexity to the analysis, underlining the importance of meticulous observation and interpretation of results.
It is noteworthy that Arachidonic Acid, the key component of this reagent, is inherently present in the granules and membranes of human platelets. When liberated from phospholipids, Arachidonic Acid undergoes a series of enzymatic transformations facilitated by cyclo-oxygenase. This process leads to the formation of prostaglandin G2 (PGG2), which is swiftly converted to prostaglandin H2 (PGH2). Ultimately, PGH2 transforms into thromboxane A2, a potent inducer of platelet aggregation.
The intricate dance of biochemical reactions orchestrated by Arachidonic Acid serves as a window into platelet physiology. Importantly, this pathway can be modulated by interventions such as aspirin, which inhibits cyclo-oxygenase-mediated oxygen consumption. As a result, the entire cascade of events leading to platelet aggregation is disrupted. This additional layer of pharmacological insight further enriches the significance of employing Arachidonic Acid Reagent in platelet studies, positioning it as a crucial asset in unraveling the complexities of platelet activation pathways.
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