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DR BILL'S PRODUCTS: NUTRIMEDS
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CELL DETOX GLUTATHIONE 1 bottle, 60 capsules each $59.95
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Glutathione
The “Master Antioxidant 

GETS RIDE OF HYDROXYL FREE RADICALS POWERFULLY VIA GLUTATHIONE PEROXIDASE ENZYMES ... !

 
•Protects the body from oxidative stress
•Maintains cellular functions
•Supports healthy immune function

MAJOR ACTIONS:
1] REMOVES HEAVY METALS
2] NUTRALIZES FOREIGN MICROBES
3] REVERSES OXIDATIVE STRESS
4] REVERSES INFLAMMATORY COMPOUNDS IN TISSUES
5] SPEEDS POST-TRAUMATIC TISSUE HEALING AND RECOVERY

CLINICAL APPLICATONS ...

 
•Provides Intracellular Antioxidant Support
•Supports Healthy Cell Function and Healthy Aging
•Supports Detoxification of Metals, Drugs, and Xenobiotics
•Supports Healthy Immune Response
•Supports Neurological, Kidney, Liver, Lung, and Eye Health
•Supports Transport of Amino Acids Across Cell Membranes
•Enhances Antioxidant Activity of Vitamins C and E


ENZYMES ACTIVATES ...

 
•Glutathione Peroxidase(GPx) catalyzes :
2GSH + H2O2 → GS–SG + 2H2O        …or….
2GSH + lipid hydroperoxide→ GS-SG + lipid alcohol

•GSH represents “reduced” monomericglutathione
•GS–SG represents “oxidized” glutathione disulfide.
•Glutathione reductasethen reduces the oxidized glutathione to complete the cycle:
GS–SG + NADPH + H+ → 2 GSH + NADP+

 GLUTATHIONE PEROXIDASE ..

•Multiple Isozymes with different locations, substrate preferences (H00H, Lipid Peroxides).  All Have GSH as co-substrate in reaction


FACTORS THAT CAN LIMIT GLUTATHIONE BIOSYNTHESIS ...

 

•Genetic enzymatic alterations
•Cysteineavailability
•Protein-calorie malnutrition
•Other dietary amino acid deficiencies
•Disease
•Chronic oxidative load can deplete levels
•Gene polymorphisms

COMMONLY USED PRECURSORS TO GLUTATHIONE ...

 
•Whey protein
•Vitamin C
•Glutamine
•NAC
–Results are inconsistent!
•Biological individuality - not every
  body has the ability to successfully metabolize the precursor to raise glutathione.

WHY NOT GIVE PURE GLUTATHIONE ?


 
•Poor compliance-most oral forms are foul smelling!

•Majority of an oral dose is oxidized before it can be absorbed and used by the cells.


S-Acetyl Glutathione Overcomes Usual Limitations ... 

 
•Unique preparation of glutathione

•Stability of S-acetylglutathionethrough the intestinal wall and the plasma is well-documented in the literature. For example:

•Vogel JU, CinatlJ, DauletbaevN,etal. Effects of S-acetylglutathionein cell and animal model of herpes simplex virus type 1 infection. Med MicrobiolImmunol(2005) 194: 55–59.
•GSH is not taken up by cells directly, but needs to be broken down into amino acids and resynthesizedto GSH intracellularly, this process often being impaired during viral infections. These obstacles may be overcome by a novel glutathione derivative
•S-acetylglutathione(S-GSH), which is more stable in plasma and taken up directly by cells with subsequent conversion to GSH. [PMID: 14624358 ]

S-Acetylglutathione is Effectively Transported Into the CELLS ....

 
Arch BiochemBiophys.1985 Jun;239(2):538-48.
•Glutathione monoethylester: preparation, uptake by tissues, and conversion to glutathione.
•Abstract
•Glutathione monoethylester (L-gamma-glutamyl-L-cysteinylglycylethyl ester), in contrast to glutathione itself, is effectively transported into many types of cells. The ester is converted intracellularlyinto glutathione. Intraperitonealinjection of 35S-labeled ester into mice was followed by rapid appearance of isotope in the glutathione of liver, kidney, spleen, pancreas, and heart; the glutathione levels of these tissues also increased. Oral administration of the ester to mice also increased cellular glutathione levels. Relatively little extracellular deesterificationwas found. Transport of glutathione ester into human erythrocytes and intracellular conversion to glutathione was observed. The findings suggest that the glutathione ester will be useful as a radioprotectingagent and in the prevention and treatment of toxicity due to certain foreign compounds and oxygen. The ester may be useful in experimental work on glutathione transport, metabolism, and function, and in related studies on oxygen toxicity, radiation, mutagenesis, and ageing. Methods for the preparation of glutathione monoethylester and several related compounds are given.
•PMID: 4004275

 MECHANISM OF ABSORPTION OF S-ACETYLGLUTATHIONE ...

 
•Lipid-like compound - taken up intact by chylomicronsin the gut
•Acetyl bond is placed on its thiolgroup or sulfur group
–Prevents oxidation
–Allows the molecule to pass diffusively into the cell

POST - GUT ABSORPTION ...

 
•Bond is cleaved by non-specific enzymes inside the cell
•Acetylationprevents breakdown of glutathione
•S-acetylglutathionedoes not require energy expenditure to be cleaved to reduced glutathione once it crosses the
    cell membrane.


S-acetylglutathionehas also been shown to decrease a variety
of inflammatory markers 



F2-Isoprostane
MDA/TBARS
H2O2
TNF-alpha


 Glutathione is the major intracellular antioxidant within the lung, liver and brain. It minimizes the impact of reactive oxygen species in the mitochondria which slows degenerative processes. A decrease in glutathione results in an increased risk of diabetes, neurological conditions, heart disease and any condition of aging

 Glutathione Peroxidaseis an endogenous antioxidant enzyme system that degrades H2O2 and is dependent on glutathione supplies.



Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide are constantly produced during metabolic processes in all living cells. Superoxide dismutase is one of the most important antioxidant enzymes systems. It protects the mitochondria and reduces degenerative processes from an over production of reactive oxygen species.

 F2-isoprostane is an eicosanoidproduced by the oxidation of phospholipids. F2 isoprostaneis a well researched marker of oxidative stress. It limits cell membrane fluidity, impacts hormone, is vasoconstrictiveand has neurologic and cardiovascular consequence.


 
•Correlates with neuroprostanes(DHA, and charged DHA does not incorporate into neurons)
•Most reliable marker of oxidative stress in vivo
•Can lead to inactivation of membrane-bound receptors or enzymes
•Decreases membrane fluidity
•Exists as an oxidative fat in plaques
•Extensive literature correlating it with neurologic, cardiovascular and carcinogenic conditions


TBARS/MDA include lipid hydroperoxidesand aldehydes, which increase as a result of oxidative stress. TBARS can be treated, and returned to normal levels, with antioxidants.

 Oxidized LDL is a highly athrogeniclipid. It is strongly correlated with risk of heart disease and other oxidative conditions.



Hydrogen Peroxide is a highly reactive oxygen species.


TNF-alpha is a cytokine that increase inflammation. It is implicated in a number of conditions including cancer, Alzheimer's, irritable bowel syndrome, depression and autism.

 Glutathione monoethylesterprevents mitochondrial glutathione depletion during focal cerebral ischemia


 
NeurochemInt.2004 Feb;44(3):153-9.
•Glutathione monoethylesterprevents mitochondrial glutathione depletion during focal cerebral ischemia.
•Source
•Centre for Neuroscience, Flinders Medical Research Institute and Department of Medical Biochemistry, School of Medicine, Flinders University, SA, Adelaide, Australia. michelle.anderson@neuro.gu.se
•Abstract
•Glutathione is a central component in the antioxidant defencesof cells. We have recently reported an early and selective loss of total (reduced plus oxidised) glutathione from mitochondria isolated from rat brain following occlusion of the middle cerebral artery. This mitochondrial glutathione depletion showed an apparent association with the tissue damage that developed during subsequent reperfusion, suggesting that it could be an important determinant of susceptibility to cell loss. In the present study, we have investigated whether in vivo treatment with glutathione ethyl ester can modulate mitochondrial glutathione in the brain and whether this treatment can influence the response to focal ischemia. In further support of our previous findings, middle cerebral artery occlusion caused a duration-dependent partial loss of mitochondrial glutathione. Bilateral injections of glutathione ethyl ester immediately prior to induction of unilateral focal ischemia resulted in a substantial increase in glutathione in mitochondria from the striatum of both the non-ischemic hemisphere (190% of saline-treated controls) and the ischemic hemisphere (240% of controls) at 2h after arterial occlusion. Total tissue glutathione was not affected by the ester treatment at this time. A smaller increase in mitochondrial glutathione was observed at 3h of occlusion in the non-ischemic striatum following ester treatment but at this time point glutathione was not significantly altered in mitochondria from the ischemic hemisphere. Pre-ischemic treatment with glutathione ester did not significantly change the volume of tissue infarction assessed at 48 h following ischemia for 2 or 3h. These studies demonstrate that glutathione ethyl ester is a highly effective modulator of the mitochondrial glutathione pool in the intact brain and provides a useful means for further investigating the role of this antioxidant in the development of tissue damage in ischemia and other brain disorders.
•PMID: 14568558

 “These studies demonstrate that glutathione ethyl ester is a highly effective
modulator of the mitochondrial glutathione pool in the intact brain and provides
 a useful means for further investigating the role of this antioxidant in the development
 of tissue damage in ischemia and other brain disorders.”


Regulation of hepatic glutathione metabolism and its role in hepatotoxicity ...

 
Exp ToxicolPathol.1996 Jul;48(5):439-46.
•Regulation of hepatic glutathione metabolism and its role in hepatotoxicity.
•Source
•Clinic of Anesthesiology and Intensive Care Medicine, General Hospital Gera, Germany.
•Abstract
•The regulation of hepatic glutathione (GSH) metabolism have been reviewed. Key steps in the regulation of hepatic GSH are GSH biosynthesis, the GSH-redox-cycle, the cystathioninepathway, and the carrier-mediated export processes. Possible influences of xenobioticson these different pathways are discussed. GSH fulfills several essential functions; detoxification of oxygen-derived free radicals, thioldisulfideexchange and storage and transfer of cysteine. GSH is present in all mammalian cells, but may be especially important for organs with intensive exposure to exogenous toxins such as the liver. Within the cell mitochondrial GSH is the main defense against physiological oxidative stress generated by cellular respiration and may be a critical target for toxins. Glutathione homeostasis of the organism is a highly complex process, which is predominantly regulated by the liver but also by skeletal muscle, lung and kidney.
•PMID: 8765689

 Within the cell mitochondrial GSH is the main defense against physiological oxidative stress
generated by cellular respiration and may be a critical target for toxins.

Augmentation of intracellular glutathione in macrophages generates and maintains appropriate Th1/Th2 balance....


 
CurrMed Chem.2006;13(15):1749-55.
•Antiviral and immunomodulatoryproperties of new pro-glutathione (GSH) molecules.
•Source
•Institute of Biological Chemistry, University of Urbino, Via Saffi, 2, 61029 Urbino(PU) Italy. magnani@uniurb.it
•Abstract
•Reduced glutathione (GSH) is present in millimolarconcentrations in mammalian cells. It is involved in many cellular functions such as detoxification, amino acid transport, production of coenzymes, and the recycling of vitamins E and C. GSH acts as a redoxbuffer to preserve the reduced intracellular environment. Decreased glutathione levels have been found in numerous diseases such as cancer, viral infections, and immune dysfunctions. Many antioxidant molecules, such as GSH and N-acetylcysteine(NAC), have been demonstrated to inhibit in vitro and in vivo viral replication through different mechanisms of action. Accumulating evidence suggests that intracellular GSH levels in antigen-presenting cells such as macrophages, influence the Th1/Th2 cytokine response pattern, and more precisely, GSH depletion inhibits Th1-associated cytokine production and/or favoursTh2 associated responses.It is known that GSH is not transported to most cells and tissues in a free form. Therefore, a number of different approaches have been developed in the last years to circumvent this problem. This review discusses the capacity of some new molecules with potent pro-GSH effects either to exert significant antiviral activity or to augment GSH intracellular content in macrophages to generate and maintain the appropriate Th1/Th2 balance. The observations reported herein show that pro-GSH molecules represent new therapeutic agents to treat antiviral infections and Th2-mediated diseases such as allergic disorders and AIDS. PMID: 16787218

 S- acetylgluthioneappears to be “selective”...


  
Cancer Lett.1996 Dec 20;110(1-2):63-70.
•Reduced glutathione and S-acetylglutathioneas selective apoptosis-inducing agents in cancer therapy.
•Source
•Department of Biological Chemistry, University Medical Center, Franfurtam Main, Germany.
•Erratum in
•Abstract
•The effect of reduced glutathione (GSH) and S-acetylglutathione(S-acglu) treatment on several tumor cell lines and normal cells in vitro was investigated. GSH and S-acgluapplied at concentrations of 1 mMand 2 mMinduced apoptosis in malignant cells as shown by DNA-fragmentation and staining of apoptotic cells with 7-amino-actinomycin D while viability and growth of normal cells were not significantly influenced by this treatment.The results demonstrated that GSH and S-acglumay be selective inducers of apoptosis in malignant cells.
•PMID: 9018082

 
Cancer Lett.1996 Dec 20;110(1-2):63-70.
•Reduced glutathione and S-acetylglutathioneas selective apoptosis-inducing agents in cancer therapy.
•Source
•Department of Biological Chemistry, University Medical Center, Franfurtam Main, Germany.
•Erratum in
•Abstract
•The effect of reduced glutathione (GSH) and S-acetylglutathione(S-acglu) treatment on several tumor cell lines and normal cells in vitro was investigated. GSH and S-acgluapplied at concentrations of 1 mMand 2 mMinduced apoptosis in malignant cells as shown by DNA-fragmentation and staining of apoptotic cells with 7-amino-actinomycin D while viability and growth of normal cells were not significantly influenced by this treatment.The results demonstrated that GSH and S-acglumay be selective inducers of apoptosis in malignant cells.
•PMID: 9018082

induced apoptosis in malignant cells as shown by DNA-fragmentation and staining of apoptotic cells with 7-amino-actinomycin D while viability and growth of normal cells were not significantly influenced by this treatment 


S- acetylgluthioneappears to be “selective”.... 


 
IntJ Oncol.2002 Jan;20(1):69-75.
•S-acetyl-glutathione selectively induces apoptosis in human lymphoma cells through a GSH-independent mechanism.
•Source
•Metastasis Research Laboratory, University of Liege, Liege, Belgium.
•Abstract
•Reduced apoptosis is associated to cancer development. Agents able to restore the programmed cell death responsiveness of cancer cells are foreseen as potential effective cancer therapies. In this study, we report that a glutathione-S-derivative, S-acetyl-glutathione (Sag), induces significant apoptosis in three human lymphoma cell lines, including Daudi, Rajiand Jurkatcells while it had no or little effect on either Hut-78 lymphoma cells or the normal BT lymphocytes. We used Annexin-V FACS analysis and DNA laddering to demonstrate that Sag activated apoptosis in the three sensitive cell lines in a dose- and time-dependent-fashion. Using mercury orange staining and FACS analysis, we showed that Sag generated an intracellular GSH depletion in Daudi, Rajiand Jurkatcells but not in Hut-78 or the normal BT cells. These data provide direct evidence that Sag specifically activates programmed cell death in lymphoma cells through, at least in part, a depletion of intracellular GSH rather than an increase, as previously suggested.Because of its selective effect on cancer cells, Sag appears as a promising new lymphoma cell apoptosis inducer with potential clinical value for lymphoma patients.
•PMID: 11743644


Because of its selective effect on cancer cells, Sag appears as a promising new lymphoma cell apoptosis inducer with potential clinical value for lymphoma patients.


 
Instructions/How to Use: Take  one capsule once to twiceto three times per day for total body detoxification of heavy metals, toxins and cellular antiaging of mitochondrial and protection of DNA.

MITOCHONDRIAL HEALTH ...

 
•S-Acetylglutathioneprovides cytosolGSH to enter the mitochondria.
–Increases mitochondrial activity
–Minimizes ROS by increasing SOD II
•Maintains mitochondrial function and integrity
 
Ingredients:

S-Acetyl Glutathione 100 mg per capsule

 PROPERTIES ...

•Orally available acetylated form of glutathione
•Patent-pending
•Stable throughout the GI tract
•Well-absorbed
•Increases intracellular glutathione
•Positive effect on many oxidative stress biomarkers
•Odor-free, tasteless
Cautions/Warnings: DOES NOT CONTAIN ...

 
•NO: wheat, gluten, corn protein, yeast, soy, animal or dairy products
•NO: artificial colors, sweeteners, or preservatives

CAUTIONS ... 
 
•Keep out of reach of children.
•Avoid if allergic to any ingredient.
Note: Drugs,suchas acetoaminophen, and alcohol, deplete glutathione and may decrease the efficacy of oral glutathione

STORAGE ...

Keep tightly closed in a cool, dry place
Conditions:

DOWNS SYNDROME Gene Doses & Support Protocols


 
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