[Trauma1]

BUMP for some more NOxidant questions or success stories!

[OCCFan023]

Just got my first bottle of NoXidant and looking forward to my first dose.

Just had a quick question. I am going to do the 3 before bed on training days, and 3 in the morning on non training days, but want to make sure I won't interfere with it with my other supplementation at the moment. Would there be any issues taking NoXidant along with my Powerfull dose before bed? I also don't see any issues taking the non workout dose with my first meal, but would there be any issues if I had taken in ReCreate or P-Slin prior to this dose.

I assume it won't matter for the later, but just wanted to confirm that its straight to take it with Powerfull.

[dsade]

no problems that I see at all.

[OCCFan023]

Originally Posted by dsade

no problems that I see at all.

Awesome, thanks DSade.

[Flyboy]

Just started noxidant last week after finally getting my shipment through.

Not really noticed any difference in my life yet, although i didn't expect to either. It's more for the long term health benefits that i'm interested in this product!

Just a note - I'm wondering if this might have some benefits (as one small part of a regime) as regards hairloss... some of the ingredients look promising in that respect. Any thoughts? What type of apple poly's do you use? procyanidin B-2 by any chance?

Cheers (oh, DCP seems awesome by the way!)

[Trauma1]

I thought this was an interesting addition to this write-up in regard to gamma-tocopherol's role in colon cancer prevention as well as inflammatory and cardiovascular disorders:


Gamma (gamma) tocopherol upregulates peroxisome proliferator activated receptor (PPAR) gamma (gamma) expression in SW 480 human colon cancer cell lines.Campbell

SE, Stone WL, Whaley SG, Qui M, Krishnan K.
Division of Hematology-Oncology, Department of Internal Medicine, East Tennessee State University and James H, Quillen VA Medical Center, Johnson City, TN 37614, USA. campbese@etsu.edu

BACKGROUND: Tocopherols are lipid soluble antioxidants that exist as eight structurally different isoforms. The intake of gamma-tocopherol is higher than alpha-tocopherol in the average US diet. The clinical results of the effects of vitamin E as a cancer preventive agent have been inconsistent. All published clinical trials with vitamin E have used alpha-tocopherol. Recent epidemiological, experimental and molecular studies suggest that gamma-tocopherol may be a more potent chemopreventive form of vitamin E compared to the more-studied alpha-tocopherol. Gamma-tocopherol exhibits differences in its ability to detoxify nitrogen dioxide, growth inhibitory effects on selected cancer cell lines, inhibition of neoplastic transformation in embryonic fibroblasts, and inhibition of cyclooxygenase-2 (COX-2) activity in macrophages and epithelial cells. Peroxisome proliferator activator receptor gamma (PPARgamma) is a promising molecular target for colon cancer prevention. Upregulation of PPARgamma activity is anticarcinogenic through its effects on downstream genes that affect cellular proliferation and apoptosis. The thiazolidine class of drugs are powerful PPARgamma ligands. Vitamin E has structural similarity to the thiazolidine, troglitazone. In this investigation, we tested the effects of both alpha and gamma tocopherol on the expression of PPARgamma mRNA and protein in SW 480 colon cancer cell lines. We also measured the intracellular concentrations of vitamin E in SW 480 colon cancer cell lines. RESULTS: We have discovered that the alpha and gamma isoforms of vitamin E upregulate PPARgamma mRNA and protein expression in the SW480 colon cancer cell lines. gamma-Tocopherol is a better modulator of PPARgamma expression than alpha-tocopherol at the concentrations tested. Intracellular concentrations increased as the vitamin E concentration added to the media was increased. Further, gamma-tocopherol-treated cells have higher intracellular tocopherol concentrations than those treated with the same concentrations of alpha-tocopherol. CONCLUSION: Our data suggest that both alpha and gamma tocopherol can upregulate the expression of PPARgamma which is considered an important molecular target for colon cancer chemoprevention. We show that the expression of PPARgamma mRNA and protein are increased and these effects are more pronounced with gamma-tocopherol. Gamma-tocopherol's ability to upregulate PPARgamma expression and achieve higher intracellular concentrations in the colonic tissue may be relevant to colon cancer prevention. We also show that the intracellular concentrations of gamma-tocopherol are several fold higher than alpha-tocopherol. Further work on other colon cancer cell lines are required to quantitate differences in the ability of these forms of vitamin E to induce apoptosis, suppress cell proliferation and act as PPAR ligands as well as determine their effects in conjunction with other chemopreventive agents. Upregulation of PPARgamma by the tocopherols and in particular by gamma-tocopherol may have relevance not only to cancer prevention but also to the management of inflammatory and cardiovascular disorders.

[Trauma1]

Another good read on the benefits of Gamma-Tocopherol:



gamma-tocopherol, the major form of vitamin E in the US diet, deserves more attention.Jiang Q, Christen S, Shigenaga MK, Ames BN.
University of California, the Department of Molecular and Cell Biology, Berkeley, USA.

gamma-tocopherol is the major form of vitamin E in many plant seeds and in the US diet, but has drawn little attention compared with alpha-tocopherol, the predominant form of vitamin E in tissues and the primary form in supplements. However, recent studies indicate that gamma-tocopherol may be important to human health and that it possesses unique features that distinguish it from alpha-tocopherol. gamma-Tocopherol appears to be a more effective trap for lipophilic electrophiles than is alpha-tocopherol. gamma-Tocopherol is well absorbed and accumulates to a significant degree in some human tissues; it is metabolized, however, largely to 2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC), which is mainly excreted in the urine. gamma-CEHC, but not the corresponding metabolite derived from alpha-tocopherol, has natriuretic activity that may be of physiologic importance. Both gamma-tocopherol and gamma-CEHC, but not alpha-tocopherol, inhibit cyclooxygenase activity and, thus, possess antiinflammatory properties. Some human and animal studies indicate that plasma concentrations of gamma-tocopherol are inversely associated with the incidence of cardiovascular disease and prostate cancer. These distinguishing features of gamma-tocopherol and its metabolite suggest that gamma-tocopherol may contribute significantly to human health in ways not recognized previously. This possibility should be further evaluated, especially considering that high doses of alpha-tocopherol deplete plasma and tissue gamma-tocopherol, in contrast with supplementation with gamma-tocopherol, which increases both. We review current information on the bioavailability, metabolism, chemistry, and nonantioxidant activities of gamma-tocopherol and epidemiologic data concerning the relation between gamma-tocopherol and cardiovascular disease and cancer.

[Trauma1]

Another GREAT read on Gamma-Tocopherol:


Enhancement of intracellular gamma-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts: relation to NO synthesis, isoprostane formation, and tocopherol oxidation.Tanaka Y, Wood LA, Cooney RV.
University of Hawaii Cancer Research Center, Natural Products and Cancer Biology Program, 1236 Lauhala Street, Honolulu, Hawaii 96813, USA. Yuichiro.tanaka@ucsf.edu

BACKGROUND: Stimulation of C3H 10T1/2 murine fibroblasts with interferon-gamma(IFN) and bacterial lipopolysaccharide (LPS) generates reactive oxygen and nitrogen species leading to DNA damage, lipid oxidation, and tocopherol oxidation. The tocopherols possess unique chemical and biological properties that suggest they have important roles related to intracellular defense against radical-mediated damage. RESULTS: Despite increased levels of reactive oxidants and decreased media tocopherol, cellular levels of gamma-tocopherol, but not alpha-tocopherol, were observed to increase significantly when cells were treated with IFN/LPS. Inhibition of nitric oxide (NO) synthesis by a specific inhibitor of inducible NO synthase (iNOS) increased both intracellular alpha-tocopherol and gamma-tocopherol concentrations, but did not significantly alter the reduction in media tocopherol levels caused by IFN/LPS treatment. Both exposure to exogenous NO and cellular synthesis of NO in cell culture increased media levels of 8-epi-prostaglandin F2alpha, a marker of oxidative lipid damage, whereas inhibition of endogenous NO synthesis reduced media 8-epi-prostaglandin F2alpha formation to control levels. CONCLUSION: Elevated intracellular levels of gamma-tocopherol in response to the cellular inflammatory state may indicate that it serves a unique role in minimizing cellular damage resulting from endogenous NO synthesis. Results of the current study suggest that NO is an important mediator of damage within the cell, as well as in the oxidation of both alpha- and gamma-tocopherols. The paradoxical increase in cellular tocopherol associated with the induction of NO synthesis may indicate either enhanced cellular transport/decreased export for tocopherols or recruitment of free tocopherol from tocopherol storage molecules.

[Trauma1]

One more! It's worth it.

This has some GREAT info on Gamma-Tocopherol and diabetes type 1 prevention:


gamma-tocopherol partially protects insulin-secreting cells against functional inhibition by nitric oxide.Sjöholm A, Berggren PO, Cooney RV.
Cancer Research Center of Hawaii, Molecular Carcinogenesis Program, University of Hawaii at Manoa, 1236 Lauhala Street, Honolulu, Hawaii, 96813-2424, USA. ake@ehk.ks.se

Preceding the onset of type 1 diabetes mellitus, pancreatic islets are infiltrated by macrophages secreting interleukin-1beta (IL-1beta) which induces beta-cell apoptosis and exerts inhibitory actions on islet beta-cell insulin secretion. IL-1beta seems to act chiefly through induction of nitric oxide (NO) synthesis. Hence, IL-1beta and NO have been implicated as key effector molecules in type 1 diabetes mellitus. In this paper, the influence of endogenously produced and exogenously delivered NO on the regulation of cell proliferation, cell viability and discrete parts of the stimulus-secretion coupling in insulin-secreting RINm5F cells was investigated. Because vitamin E may delay diabetes onset in animal models, we also investigated whether tocopherols may protect beta-cells from the suppressive actions of IL-1 and NO in vitro. To this end, the impact of NO on insulin secretory responses to activation of phospholipase C (by carbamylcholine), protein kinase C (by phorbol ester), adenylyl cyclase (by forskolin), and Ca(2+) influx through voltage-activated Ca(2+) channels (by K(+)-induced depolarization) was monitored in culture after treatment with IL-1beta or by co-incubation with the NO donor spermine-NONOate. It was found that cell proliferation, viability, insulin production and the stimulation of insulin release evoked by carbamylcholine and phorbol ester were impeded by IL-1beta or spermine-NONOate, whereas the hormone output by the other secretagogues was not altered by NO. Pretreatment with gamma-tocopherol (but not alpha-tocopherol) afforded a partial protection against the inhibitory effects of NO, whereas specifically inhibiting inducible NO synthase with N-nitro-L-arginine completely reversed the IL-1beta effects. In contrast, inhibiting guanylyl cyclase with ODQ (1H-[1,2, 4]oxadiazolo[4,3-alpha]-quinoxaline-1-one) or blocking low voltage-activated Ca(2+) channels with NiCl(2) failed to influence the actions of NO. In conclusion, our data show that NO inhibits growth and insulin secretion in RINm5F cells, and that gamma-tocopherol may partially prevent this. The results suggest that phospholipase C or protein kinase C may be targeted by NO. In contrast, cGMP or low voltage-activated Ca(2+) channels appear not to mediate the toxicity of NO in these cells. These adverse effects of NO on the beta-cell, and the protection by gamma-tocopherol, may be of importance for the development of the impaired insulin secretion characterizing type 1 diabetes mellitus, and offer possibilities for intervention in this process.

[dsade]

That Urine excretion note is highly interesting, as it sets me wondering about free radical roles in kidney damage, and the possible prevention with the unique structure of gamma-tocopherol and its metabolites.

[Trauma1]

Originally Posted by dsade

That Urine excretion note is highly interesting, as it sets me wondering about free radical roles in kidney damage, and the possible prevention with the unique structure of gamma-tocopherol and its metabolites.

This is most definitely a point of interest. Gamma-Tocopherol is proving to be the antioxidant of primary interest in not only specific, but systemic disease prevention. If much of what these studies holds true, a powerful supportive treatment for disease prevention is on the horizon.

RPN's NOxidant is on par (and even bests) the vast majority of effective antioxidant protection supplements on the market for the price.