what is l-glutathione, and what effect does it have on you?
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Mega L-Glutathione Capsules\n250 mg, 60 capsules\nItem Catalog Number: 314 \nL-cysteine is a conditionally essential amino acid, one of only three sulfur-containing amino acids, the others being taurine (which can be produced from L-cysteine) and L-methionine from which L-cysteine can be produced in the body by a multi-step process. Cysteine plays a role in the sulfation cycle, acting as a sulfur donor in phase II detoxification and as a methyl donor in the conversion of homocysteine to methionine. Cysteine also helps synthesize glutathione, one of the body’s most important natural detoxifiers. N-acetyl-cysteine is the acetylated form of L-cysteine, which is more efficiently absorbed and used.54-64\n\nGlutathione (gamma-L-glutamyl-L-cysteinyl-glycine) is a peptide (short protein)-like molecule synthesized in the body from the three amino acids L-glutamic acid, L-cysteine, and glycine. Glutathione is one of the body’s most important and powerful antioxidants, helping to detoxify xenobiotics. A major function of vitamin C is to keep glutathione in its reduced form so that they can continue to provide free radical quenching effects.65-68\n\nEven though many published studies show that garlic, selenium, alpha-lipoic acid, L-cysteine, and N-acetyl-cysteine can boost cellular glutathione levels, people with health problems may benefit from taking high doses of glutathione.65,69-71*\n \nReferences  \nSupplement Facts \nServing Size 1 capsule\n \nServings Per Container 60\n \nAmount Per Serving \nL-glutathione\n 250 mg\n \nOther ingredients: gelatin, cellulose, purified water, magnesium stearate, silica.\n \n \nDosage and Use \n  Take one capsule daily, preferably with a meal.\n \n \nCaution \nWhen taking L-cysteine, N-acetyl-cysteine, or glutathione, it is recommended that three times as much vitamin C should be taken at the same time to prevent these amino acids from being oxidized in the body
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AST, ALT, SGOT, SGPT, and GGT and Alkaline Phosphatase are abbreviations for proteins called enzymes. Injury to cells release these enzymes into the blood. They are found in muscles, the liver and heart. Damage from alcohol and a number of diseases are reflected in high values.\nAlkaline phosphatase is an enzyme found primarily in bones and the liver. Expected to be higher for those who are growing (children and pregnant women) or when damage to bones or liver has occurred or with gallstones. GGT is also elevated in liver disease, particularly with obstruction of bile ducts. Unlike the alkaline phosphatase it is not elevated with bone growth or damage.AST/SGOT , ALT/ SGPT are also liver and muscle enzymes. They may be elevated from liver problems, hepatitis, excess alcohol ingestion, muscle injury and recent heart attack.LDH is the enzyme present in all the cells in the body. Anything which damages cells, including blood drawing itself, will raise amounts in the blood. If blood is not processed promptly and properly, high levels may occur. If all values except LDH are within expected ranges, it is probably a processing error and does not require further evaluation.Bilirubin: is a pigment removed from the blood by the liver. If low are of no concern. If slightly elevated above the expected ranges, but with all other enzymes (LDH, GOT, GPT, GGT) within expected values, it is probably a condition known as Gilbert’s syndrome and is not significant CPK is an enzyme which is very useful for diagnosing diseases of the heart and skeletal muscle. This enzyme is the first to be elevated after a heart attack (3 to 4 hours). If CPK is high in the absence of  heart muscle injury, this is a strong indication of skeletal muscle disease.
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It is hypothesized that the inhibitory effect ubiquinone has on NF-kB, a major regulator of immune response and a primary transcription factor for anti-oxidant enzymes, is due to the reduction of oxidant stimulation.  Ubiquinone is involved in a large number of pathways, so you would have to be more specific than merely antioxidant.
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it depends on how much mercury youve been exposed to. if it was a lot, then yes, you may possibly have long-term affects. go see your doctor if you are unsure. i hope you are OK.\nGOOD LUCK!!!
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Effect of enzyme on reaction
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Lots of good, little harm.  It acts as an antioxidant and has been shown beneficial to the cardiovascular system, and also may help with diabetes and breast cancer.  Note:  By little harm, I mean that none of my sources show any long-term harm.  Only short-term side effects such as stomach upset and headache.
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If you can prove the answer to your question you will win a Nobel Prize!  Research is accumulating that strongly suggests that homocysteine may be harmful.  But ... it is still possible that it is merely a biomarker for methylation problems and/or other problems related to its metabolism (e.g. cysteine production).
439642
nope, it seriuosly damages your digestive system if prolongly used
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They react with oxidant molecules and free radicals that are present inside your body. Highly oxidant molecules otherwise react with proteins and cellular components, that can damage cells.\n\nSo antioxidants help to protect your cells.
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monosodium glutamate; flavor enhancer.  It is free glutamate.  Glutamate is an amino acid that is in many of the proteins in your body.  In proteins, it's bound to other amino acids.  MSG is an unbound form of glutamate.\n\nBy the way, aspartame, the artificial sweetener, contains phenylalanine, another amino acid that most people have in their bodies.
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Antioxidants are best known for their action as a radical oxygen species scavenger.  Radical oygen species can deteriorate the membranes of cells in the body, and people suspect that part of the aging process is due to an accumulation of radical oxygen species over time.
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Prednisone is a glucocorticoid(type of corticosteroid)\n\n) Metabolic Effects = catabolic\nCarbohdrate \n-Generally catabolic, stimulates the formation of glucose\n (Protein is degraded for gluconeogenesis, negative nitrogen balance -nitrogen excretion results)\n-Decreases utilization of glucose in peripheral tissues\n(insulin release occurs as a homeostatic response to the rise in blood glucose)\n-Increases blood glucose -protecting glucose-dependent brain function\n\nTHESE DEPLETED STORES LEAD TO INCREASE DEMAND--HENCE INCREASED APPETITE
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ANTIOXIDANTS \n\nThese are used to prevent rancidity in fatty foods and to protect the fat-soluble vitamins (A, D, E, and K) against damage by oxidation. Synthetic antioxidants include esters of gallic acid, butylated hydroxytoluene, and butylated hydroxyanisole. Vitamins C and E are also commonly used as antioxidants; they obviously enhance the nutritional value of the food to which they are added; indeed, there is some evidence that synthetic antioxidants used in food manufacture also have useful antioxidant action in the body.\n\n\n\n\nFREE RADICALS, any molecule capable of independent existence that contains one or more unpaired electrons. An unpaired electron is one that occupies an atomic or molecular orbital by itself. A free radical can be regarded as a fragment of a molecule; free radicals are often extremely reactive, and therefore short-lived.\n\nOrganic free radicals were recognized by Gomberg in 1900 and this led to speculation that free radical species might play a role in biology. In 1966 Slater proposed that a free radical reaction was the cause of carbon tetrachloride's toxic effect on liver cells, and the theory that free radicals play a role in tissue damage was born.\n\nFree radicals are produced in most cells of the body as a byproduct of metabolism, although some cell types manufacture larger quantities for specific purposes (for example, by macrophages during phagocytosis. see Immune System). The most important free radicals found in aerobic cells, such as those in humans, are oxygen, superoxide, hydroxyl radical, hydrogen peroxide, and the transition metals. When free radicals form within cells they can oxidize biomolecules (molecules used inside cells, especially lipids) and thus cause cell death and injury. However, the human body has developed various mechanisms in order to protect itself from the damaging effects of free radicals. There are enzymes which decompose peroxides and transition metals; other free radicals are sequestered by proteins and other molecules.\n\nFree radicals are difficult to study because they are only present for very short periods. They usually react with other molecules very quickly. In recent years, it has become accepted that they play an important part in several medical conditions. DNA (see Nucleic Acids) is particularly susceptible to oxidation by free radicals and it has been suggested that these substances may have a role to play in the mutations which precede the development of cancer. This may explain why some transition metals, such as nickel and chromium, are carcinogenic under certain circumstances. Free radicals have also been implicated in atherosclerosis, liver damage, lung disease, kidney damage, diabetes mellitus, and ageing. It is not always easy to tell if free radicals are the cause of a disorder or a result of some other causative agent.\n\n\n\nVirus (biology)\nI  INTRODUCTION \n\nVirus (biology) (Latin, “poison”), any of a number of organic entities consisting simply of genetic material surrounded by a protective coat. The term “virus” was first used in the 1890s to describe agents that caused diseases but were smaller than bacteria. By itself a virus is a lifeless form, but within living cells it can replicate many times and harm its host in the process. The hundreds of known viruses cause a wide range of diseases in humans, other animals, insects, bacteria, and plants (see Diseases of Animals).\n\nThe existence of viruses was established in 1892, when Russian scientist Dmitry I. Ivanovsky discovered microscopic particles later known as the tobacco mosaic virus. The name virus was applied to these infectious particles in 1898 by the Dutch botanist Martinus W. Beijerinck. A few years later, viruses were found growing in bacteria; these viruses were dubbed bacteriophages. Then, in 1935, the American biochemist Wendell Meredith Stanley crystallized tobacco mosaic virus and showed that it is composed only of the genetic material called ribonuc
353146
It is an enzyme that can counteract the damagging effects of oxygen in tissues. Like the vitamin E.
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*****Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen.\n\nElevated levels of homocysteine are associated with an increased risk of atherosclerosis and thrombosis. The reactivity of the sulfhydryl group of homocysteine has been implicated in molecular mechanisms underlying this increased risk. There is also increasingly compelling evidence that thiols react in the presence of nitric oxide (NO) and endothelium-derived relaxing factor (EDRF) to form S-nitrosothiols, compounds with potent vasodilatory and antiplatelet effects. We, therefore, hypothesized that S-nitrosation of homocysteine would confer these beneficial bioactivities to the thiol, and at the same time attenuate its pathogenicity. We found that prolonged (> 3 h) exposure of endothelial cells to homocysteine results in impaired EDRF responses. By contrast, brief (15 min) exposure of endothelial cells, stimulated to secrete EDRF, to homocysteine results in the formation of S-NO-homocysteine, a potent antiplatelet agent and vasodilator. In contrast to homocysteine, S-NO-homocysteine does not support H2O2 generation and does not undergo conversion to homocysteine thiolactone, reaction products believed to contribute to endothelial toxicity. These results suggest that the normal endothelium modulates the potential, adverse effects of homocysteine by releasing EDRF and forming the adduct S-NO-homocysteine. The adverse vascular properties of homocysteine may result from an inability to sustain S-NO formation owing to a progressive imbalance between the production of NO by progressively dysfunctional endothelial cells and the levels of homocysteine.\n\n\n\n\n\n\n********Characterization of the stress-inducing effects of homocysteine.\n\n\nThe mechanism by which homocysteine causes endothelial cell (EC) injury and/or dysfunction is not fully understood.\n\nhomocysteine increases the expression of GRP78 and GADD153, stress-response genes induced by agents or conditions that adversely affect the function of the endoplasmic reticulum (ER). \n\nstudies indicate that the activation of stress response genes by homocysteine involves reductive stress leading to altered ER function and is in contrast with that of most other EC perturbants. The observation that homocysteine also decreases the expression of the antioxidant enzymes glutathione peroxidase and natural killer-enhancing factor B suggests that homocysteine could potentially enhance the cytotoxic effect of agents or conditions known to cause oxidative stress.\n\nPls refer to: \n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=8380812&dopt=Abstract\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9576870&dopt=Abstract
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you mean antioxidants...
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The bodies natural ability to heal and repair itself is aided with glconutrient supplementation.\n\nI will tell you what to take. It is safe and natural.