Pure Healing

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The role of redox signaling molecules against Hepatite C Virus

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One of our Associates have been trying to help a Hep-C group to understand Redox Balance. He posted something about Redox Signaling and one person commented with:

“At the end of the day we get all the help we can from humans eh but our ultimate help comes from God…”

So This is our Associate’s reply…Tell me what you think !

Reply:

I disagree Donna…we need to help ourselves by educating ourselves with the mounting knowledge that science has documented over the last 100 years and the new discoveries that are being made everyday.
If you know how Hep-c is allowed to form and replicate in the body then you are starting at the root of the disease. All the studies that I have read..and have have lots from all over the world going back many years point directly to oxidative stress as the catalyst for the progression of the disease. This leads to a redox imbalance which allows free radicals to attack the liver. Redox imbalance is when the body is not producing the exact amount of Oxidents and Reductants thus the body can not control free radicals cased by Oxdative stress. Which in turn allows Apoptosis (planned cell kill). As this starts to happen in the cell then the body can not utilize the 3 super enzymes in the body that fire antioxidents to fight back. They are Glutathione, Super Oxide Dismutase (Sod) or (ATP) and Catalase. These molecules are responsible for detoxifying, turning minerials (sugars) into energy and rebuilding damaged tissue on a cellular level and this is all done by proper Redox Signaling in all living things.

This is the down hill progrestion the cells go through when the body is in a state of Redox Imbalance.
Hepatitis C virus (HCV) is a major cause of viral hepatitis. Oxidative stress is emerging as a key step and a major initiator in the development and the progression of liver damage, and the evaluation of oxidative stress may be useful for a better understanding of the pathogenesis of hepatitis.

Patients infected with HCV showed increased serum lipid peroxidation (LPO) products due to breakdown of the polyunsaturated fatty acids in the cell membranes, endoplasmic reticulum, and mitochondria. LPO leads to oxidative destruction of polyunsaturated fatty acids constitutive of cellular membranes. Their destruction leads to the production of toxic and reactive aldehyde metabolites such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE). These highly cytotoxic metabolites, produced in relatively large amounts, can diffuse from their site of origin to attack distant targets and form covalent bonds with various molecules. The augmented oxidative stress may possess diverse effects on cell growth and later on induce apoptosis.

Furthermore, studies have indicated that HCV can directly induce oxidative stress intracellularly in hepatocytes. HCV core gene expression has been associated with increased ROS, decreased intracellular, and/or mitochondrial glutathione (GSH) content, and increased levels of oxidized thioredoxin and LPO products. The molecular mechanism of how the HCV core protein induces oxidative stress has been investigated. The core protein has now been shown to associate with the outer mitochondria membrane via its COOH-terminal region. Previously, the increased ROS generation with HCV core protein was shown to be inhibited with diphenyliodonium, on the basis of this finding, the core protein was suggested to stimulate ROS production by the electron transport chain of mitochondria.

In addition, chronic HCV infection is associated with decreased plasma levels of the antioxidant contents due to their inefficient intracellular synthesis. Therefore, host antioxidant defenses, such as GSH, catalase, superoxide dismutase (SOD), and hemo-oxygenase-1 are subnormal in Chronic hepatitis C (CHC) disease. These HCV-induced Redox reactions can occur through multiple liver injury mechanisms that include chronic inflammation, activated Kupffer cells, and iron overload. In health, cellular Redox environment is tightly regulated by antioxidants that directly catalyze the unneeded oxidants or reverse their structural chemistry. There is a reverse correlation between level of severity of HCV infection and blood antioxidant levels. Therefore, antioxidant supplement is highly supportive against this disease.
So knowing the how and why of Hep-c…..then maybe you can understand that this product called Asea that I am using is a 100% native to the body and a perfectly balanced set of Oxidants and Reductants for supplementing the bodies diminishing supply of Redox Signaling Molecules. The #1 fact you need to know about Asea is that all research has shown that using Asea increases bio-availibilty and effectiveness of the body`s natural production of glutathione, as well as Super Oxide Dismutase (SOD) and Catalase by 500% and some studies show as high as 800%. This is the help we need to deal with the symptoms of this disease and the side effects that we are left with after doing this government regulated “TREATMENT”. I am living proof that if the body starts working again then we get our lives back. We come into this world alone and we go out the same…I think we need to look within us 🙂

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