This sulfhydryl-reducing agent (glutathione) is a tripeptide containing cysteine that occurs in millimolar concentrations in most cells, where it acts as a detoxifying agent, assists amino acid transport and quenches free radicals, in addition to regulating the internal redox environment of cells.
Together with ascorbates, GSH participates in the regeneration of vitamin E which emphasises the cooperation of antioxidants. Reduced GSH reacts directly with singlet oxygen, hydroxyl radicals and superoxide radicals to form oxidised glutathione (GSSD). With aging, there is a general decline in GSH levels and low GSH levels are associated with a variety of chronic conditions such as diabetes, age related macular degeneration, gastrointestinal disorders and neurodegenerative disease.
GSH S-transferase adds GSH to potentially toxic substances and is considered a component of Phase II detoxification enzymes. It also functions in the synthesis of prostaglandins and leukotrienes.
GSH synthesis is regulated in part by cysteine availability. As a supplement, n-acetylcysteine is an effective precursor for GSH. It is deacetylated in the gut to free cysteine and all supplementation can effectively raise intracellular GSH in model systems and in healthy individuals. NAC will be expected to play a supporting role to improve GSH status and maintain cell redox balance, counter free radicals and attenuate drug toxicity as a conjugating agent in drug metabolism. A primary detoxification route is the conjugation of glutathione and to recap, this is a tripeptide composed of three amino acids; cysteine, glutamic acid and glycine. The liver enzyme glutathione S-transferase takes sulphur and GSH and combines (conjugates) it with the toxic substance, making it water soluble. This water soluble form called a mercaptate is then excreted in the urine. In order to function, glutathione S-transferase needs plenty of glutathione.
GSH is also an important antioxidant in the cellular mitochondria, the energy production factories of the cell. Cellular mitochondrion glutathione is our main defence against free radicals produced as a by-product of cellular respiration, i.e. the production of energy in the cells from oxygen and fuel. In addition, glutathione is an important neutraliser of free radicals produced when the liver neutralises toxins through the Phase I pathway. GSH appears to be especially important in organs exposed to toxins such as the liver, kidney, lungs and intestines. The combination of detoxification and free radical protection results in glutathione being one of the most important anti-carcinogens and antioxidants in our cells which means that a deficiency is devastating.
When we are exposed to high levels of toxins, GSH is used up faster than it can be produced or absorbed from the diet. We then become much more susceptible to toxin induced diseases such as cancer, Lyme disease and heavy metal burden, especially if our Phase I detoxification system is highly active. An example of heavy toxin loads can be looked at in relation to pesticides and also alcohol. The alcohol increases the rate of formation of activated intermediates from the pesticides by Phase I, but the depletion of glutathione means these toxins hang around longer and more free radicals are released, causing more damage, this time to the liver, brain and nervous system.
GSH is available through two routes, diet and synthesis. Dietary glutathione found in fresh fruits and vegetables, cooked fish and meat, is absorbed well by the intestines and does not appear to be affected by the digestive processes. Beside supporting Phase II detoxification dietary glutathione appears to also detoxify substances in the intestine before they can be absorbed into the bloodstream.
GSH is incredibly useful for brain inflammation which is often caused by toxins such as heavy metals or mycotoxins. Therefore, we believe that using glutathione as part of a chronic health treatment regimen is incredibly important. The problems that arises is that oral use of glutathione does not seem to be very well readily absorbed, even with the liposomal products. It is our estimation that liposomal glutathione orally may be at best only 15-20% absorbed. This then leaves two other options, one of which is intravenous glutathione which we are able to provide at the cheapest rates in London in our clinic. For those that cannot reach the clinic or for ongoing maintenance we now have available suppository forms of glutathione which are incredibly well absorbed.