How the hyperbaric oxygen regulating NADPH facilitates the vascular health
The hyperbaric oxygen and GT Rac1 always plays a very central role in the activation of the complex. The Rac1 regulates the actin cytoskeleton as it responds to the various signals. When the NADPH is stimulated either by mechanical factors or by the signaling of the molecules, the Rac1 dissociates from its inhibitor and it is consequently activated by the release of the GDP and the binding GTP which in turn exposes the isoprenyl moiety ( Seyfried, T. N. 2012). This therefore agglomerates the cytosolic components of the NADPH oxidase NOXA1 and NOXO1. The end process therefore results to the release of a signaling molecule H2O2 through the catalytic activity of Cu and Zn-superoxide dismutase (SOD). The action of the hyperbaric oxygen on the NADPH is a multi-facet regular of the cellular functions (Naheedy et al, 2014). The action of the hyperbaric oxygen on the regulation of the NADPH oxidase is directly corresponds to the control of the cellular motility thus in the long run contributes greatly to the vascular health. This is done directly since the hyperbaric oxygen facilitates the growth and development of the vascular cells.
How the hyperbaric oxygen regulating mitochondrial oxygen species facilitates the vascular health
The mitochondria is always well known for the major roles that it plays in the body of an organism such as the production of ATP, homeostasis of Calcium and the biosynthesis of steroid and heme. However, the reactive oxygen species of the mitochondria (ROS) are always toxic products that inhibits the physiologic activities of the mitochondria facilitation of the vascular health. The hyperbolic oxygen regulates the mitochondria reactive oxygen as described in the process hereafter: Since the mitochondria acts as the cellular power plant, it therefore converts the energy that is carried by the nutrients to ATP, through the oxidative phosphorylation. The mitochondrial reactive oxygen species always regulate the important vascular homeostatic functions which are under the basal conditions for a variety in the vascular beds (Korthuis, R,2011).They are very important since they highly contribute to the endothelium dependent vasodilation. This therefore implies that the regulation of the mitochondrial oxygen by the hyperbolic oxygen directly contributes to the facilitation of the vascular health. More energy is supplied to the vascular cells thus facilitating its health.
One of the major and most fatal contributor to the brain injuries is the oxidative stress and subarachnoid hemorrhage (SAH) and the major source of the enzyme production of superoxide anion in the brain is the NADPH. There has been a study on whether therefore the hyperbolic oxygen also abbreviated as (HBO) also suppresses the neuronal NADPH oxidase. This research specimen for this experiment was a rat (Naheedy et al, 2011). As the process continues, a pair of electrons is normally donated by the NADPH to the complex I which is the NADPH-ubiquinone oxidoreductase or by the FADH2 to the complex 2 which is also known as the succinate dehydrogenase. This is of the electron transport chain, the ETC which is in the inner membrane of the mitochondria. The electrons are afterwards carried along the electron transport chain in the order of the complexes and are then afterwards accepted by the cytochrome c oxidase (Mandelker et al, 2011).
This process undergoes through four electron reduction of the oxygen thus the product of the process is water. After the electrons are have flown down to the complexes, then the energy that is released is always used for the translocation of the protons from the mitochondrial matrix to the inter-membrane space. This leads to the creation of the proton gradient, also known as mitochondrial membrane potential. Conclusively, the hyperbaric oxygen regulating NADPH and the mitochondrial reactive oxygen species therefore facilitates vascular health.
Work cited
Seyfried, T. N. (2012). Cancer as a metabolic disease: On the origin, manage
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Korthuis, R. J. (2011). Skeletal muscle circulation. San Rafael, Calif: Morgan & Claypool Life Sciences.
Mandelker, L., & Vajdovich, P. (2011). Studies on veterinary medicine. New York: Humana Press/Springer.
Naheedy, J. H., & Orringer, D. A. (2010). Deja review.
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