Study finds IL-2 reduces cancer proliferation and metastasis; however, mistletoe alone found to stimulate proliferation, though at very low doses i.e. 1 ng/kg, in mouse model.
Studies have debated on the proxidant/antioxidant effect of high dose IV vitamin C. This study finds only antioxidant effects from IV vitamin C in vivo. This study also found the antioxidant effect plateaued out at 25 grams.
subnormal plasma ascorbic acid levels are a predictable feature in patients with severe sepsis
Ascorbic acid depletion in sepsis results from ascorbic acid consumption by the reduction of plasma free iron, ascorbic acid consumption by the scavenging of aqueous free radicals (peroxyl radicals), and by the destruction of the oxidized form of ascorbic acid dehydroascorbic acid
Sepsis further inhibits intracellular reduction of dehydroascorbic acid, producing acute intracellular ascorbic acid depletion
Ascorbic acid treated patients in this study exhibited rapid and sustained increases in plasma ascorbic acid levels using an intermittent every six hours administration protocol
Septic ascorbic acid-deficient neutrophils fail to undergo normal apoptosis. Rather, they undergo necrosis thereby releasing hydrolytic enzymes in tissue beds, thus contributing to organ injury
We speculate that intravenous ascorbic acid acts to restore neutrophil ascorbic acid levels
Repletion of ascorbic acid in this way allows for normal apoptosis, thus, preventing the release of organ damaging hydrolytic enzymes.
Study finds IV vitamin C in patients with sepsis is very safe and blunts the effects (endothelial damage, end organ damage...) of sepsis. Of note, the IV vitamin C group reached serum levels of ascorbic acid of 1,592 to 5,722 micromol/L. The IV groups maintained elevated serum C levels for up to 96 hours post infusion.
diet enriched in fruits and vegetables (and consequently phytochemicals) was able to reverse the process and maintain and even elevate insulin sensitivity and glucose tolerance
LPS-mediated effects are related to an increase in TLR4 levels that triggers the activation of nuclear factor-kB (NF-kB), a transcription factor that activates a cascade of inflammatory mediators [41]. These factors control the transcription of inflammatory mediators, such as IL-1β, IL-6, TNF-α, TNF-β, INF-α, INFβ, INF-γ
Inflammation can alter insulin action and give rise to diabetes and obesity by blocking insulin receptor downstream events, impairing insulin receptor substrate 1 (IRS-1) activation and phosphatidylinositol 3-kinase-dependent (PI3K) pathways, therefore compromising insulin signaling
systemic inflammation (generated by LPS) also increased neopterin levels in the urine and resulted in altered neuronal activity by decreasing dopamine (DA) metabolism
an increase in neopterin levels has been recognized a sensitive biomarker for immune system activation
Our experiments denoted that these diets were able to diminish inflammatory mediators and oxidative damage
O3 not only remedied infection, but also had hemodynamic and anti-inflammatory properties
Stimulation of oxygen metabolism
In fungi, O3 inhibits cell growth at certain stages
With viruses, the O3 damages the viral capsid and upsets the reproductive cycle by disrupting the virus-to-cell contact with peroxidation.
Inactivation of bacteria, viruses, fungi, yeast and protozoa: Ozone therapy disrupts the integrity of the bacterial cell envelope through oxidation of the phospholipids and lipoproteins
Activation of the immune system
30 and 55 μg/cc
production of interferon and the greatest output of tumor necrosis factor and interleukin-2
Mechanism of action of O3 on the human lung
cascade of reactions like peroxidation of lipids leading to changes in membrane permeability,[41] lipid ozonation products (LOP) act as signal transducer molecules
Dietary antioxidants or free radical scavengers like vitamin E, C, etc., can prevent aforementioned effects of O3