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Estrogen & the Immune System: Of Mice and Women and Nitric Oxide
Nitric Oxide synthases catalyze conversion of L-arginine to L-citrulline and Nitric Oxide
Being a women can be both a disadvantage and an advantage, when you are talking about the immune system. It’s well known that both adaptive immune responses and innate responses of women are more robust than men.
But women are more predisposed to autoimmune disorders such as multiple sclerosis, rheumatoid arthritis, and lupus. Estrogen can cause physiological effects such as proliferative endometrium, increased body fat, cyclical migraines, thyroid hormone functions and increased risk of blood clots. These gender distinctions are mainly associated to estrogen levels. Estrogen associated management of Nitric Oxide, and the enzymes which create it, progressively emerge to take on an essential function.
Nitric Oxide synthases (NOS) catalyze the conversion of L-arginine to L-citrulline and Nitric Oxide. Dendritic cells, macrophages, and NK cells create both inducible and endothelial types, iNOS and eNOS, with iNOS producing the greatest Nitric Oxide levels.
Nitric Oxide production
Nitric Oxide manufacturing is balanced by numerous devices, consisting of control of calcium, arginases, co-factors (FAD, FMN, heme, and calmodulin), dimerization, feedback policy, iNOS induction, and protein security. The activities of Nitric Oxide are very hard to identify, considering that Nitric Oxide is a labile and extremely diffusible gas that takes numerous forms.
Nitric Oxide has concentration-dependent anti-microbial, anti-apoptotic activities, anti-inflammatory, and regulates chemokine and cytokine manufacturing in particular cell types and settings.
Current information explains one method that estrogen stimulates Nitric Oxide manufacturing in mouse spleen. Estrogen therapy in vivo enables profound Nitric Oxide manufacturing by isolated splenocytes, provided 3 conditions are fulfilled. First, T cells require stimulation, for instance by the T cell mitogen ConA or by CD3 antibodies.
Second, co-stimulation by an antigen-presenting cell is needed, because CTLA-4 Ig blocks both the B7/CD28 communication and Nitric Oxide manufacturing. Third, T cell manufacturing of IFN-gamma is needed, considering that absence of Nitric Oxide manufacturing by IFN-gamma-/- splenocytes is restored by exogenous IFN-gamma.
Keywords: nitric oxide, nitric oxide (NO), Estrogen, Immune System, autoimmune disorders, multiple sclerosis, rheumatoid arthritis, lupus, estrogen levels, Nitric Oxide synthases (NOS), Nitric Oxide synthases, L-arginine, L-citrulline, Nitric Oxide levels
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