GLUTATHIONE

Glutathione (GSH) is an important antioxidant in plants, animals, fungi, and some bacteria and archaea. Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals.

Glutathione is not an essential nutrient for humans, since it can be synthesized in the body from the amino acids L-cysteine, L-glutamic acid, and glycine; it does not have to be present as a supplement in the diet. Still, GSH synthesis in the liver has been shown to be essential. The body makes its own glutathione and does not absorb ingested supplements. Lyposomal glutathione may be taken, but has side effects to be kept in mind.





















Glutathione has multiple functions:


  • GSH levels in cells is becoming a predictor of how long we will live
  • Maintains levels of reduced glutaredoxin and glutathione peroxidase
  • One of the major endogenous antioxidants produced by the cells, participating directly in the neutralization of free radicals and reactive oxygen compounds, as well as maintaining exogenous antioxidants such as vitamins C and E in their reduced (active) forms
  • Nitric oxide cycle regulation critical for life
  • Used in metabolic and biochemical reactions such as DNA synthesis and repair, protein synthesis, prostaglandin synthesis, amino acid transport, and enzyme activation. Every system in the body can be affected by the state of the glutathione system, especially the immune system, the nervous system, the gastrointestinal system, and the lungs
  • Has a vital function in iron metabolism. Yeast cells depleted of GSH or containing toxic levels of GSH show an intense iron starvation-like response and impairment of the activity of extramitochondrial ISC enzymes thus inhibiting oxidative endoplasmic reticulum folding, followed by death
  • Has roles in progression of the cell cycle, including cell death. GSH levels regulate redox changes to nuclear proteins necessary for the initiation of cell differentiation. Differences in GSH levels also determine the expressed mode of cell death, being either apoptosis or cell necrosis. Manageably low levels result in the systematic breakage of the cell whereas excessively low levels result in rapid cell death


GSH helps the liver detoxify fat before bile is emitted, which takes stress off of the gall bladder. It is a helper molecule for important enzymes and is involved in critical biogenesis of 1/3 of all human proteins. It reduces peroxides, participates in leukotriene production, it helps detox toxins produced as by-products of metabolism, and cancer programmed cell death. GSH plays a crucial role in immune function, promotes T-cell function, prevents drug resistance, protects from environmental toxins, and fights cancer. In fact, elevated GSH levels in tumor cells are able to protect such cells in bone marrow, breast, colon, larynx, and lung cancers. Adversely, GSH deficiency causes cells to be more vulnerable to oxidative stress which contributes to cancer development. A growing number of researchers are crediting the increase in neurological disease and cancer to glutathione deficiency.





















Experts now recognize that an alarming rate of people are GSH deficient because of:


  • Pre-mature aging
  • Infections
  • Chronic stress
  • Injuries
  • Environmental toxins
  • So-called “health foods”
  • Genetically modified foods
  • Artificial sweeteners
  • Overuse of antibiotics
  • Radiation therapy that is all too easily given to cancer patients today
























How to boost GSH production:


To boost GSH production, the following processes are recommended:


  • Calcitriol, the active metabolite of vitamin D3, after being synthesized from calcifediol in the kidney and by liver, increases glutathione levels in the brain and appears to be a catalyst for glutathione production. It takes about ten days for the body to process vitamin D3 into calcitriol. S-adenosylmethionine (SAMe), a co-substrate involved in methyl group transfer, has also been shown to increase cellular glutathione content in persons suffering from a disease-related glutathione deficiency
  • Milk thistle
  • Arugula, Bok Choy, broccoli, Brussel sprouts, cabbage, cauliflower, collard and mustard greens, kale, radish, turnip, watercress
  • N-acetyl cysteine
  • α-Lipoic Acid
  • Vitamins B6, B9, B12, and biotin
  • Vitamins C and E
  • Selenium
  • L-cysteine, L-glutamic acid, and glycine
































Deficiency:


Glutathione deficiency is found in nearly all very ill patients. These include people with chronic fatigue syndrome, heart disease, cancer, chronic infections, autoimmune disease, diabetes, autism, Alzheimer's disease, Parkinson's disease, arthritis, asthma, kidney problems, liver disease and more. Normally glutathione is recycled in the body - except when the toxic load becomes too great. And that explains why we are in such trouble. That is why most people survived with the basic version of the genetic detoxification software encoded in our DNA, which is mediocre at ridding the body of toxins. At the time humans evolved we just didn't need more. Who knew we would be poisoning ourselves and eating a processed, nutrient-depleted diet thousands of years later? These people are missing GSTM1 function - one of the most important genes needed in the process of creating and recycling glutathione in the body.


Mutations in the GSS gene cause glutathione synthetase deficiency. The GSS gene provides instructions for making an enzyme called glutathione synthetase. This enzyme is involved in a process called the gamma-glutamyl cycle, which takes place in most of the body's cells. This cycle is necessary for producing a molecule called glutathione. Glutathione protects cells from damage caused by unstable oxygen-containing molecules, which are byproducts of energy production. Glutathione is called an antioxidant because of its role in protecting cells from the damaging effects of these unstable molecules. Mutations in the GSS gene prevent cells from making adequate levels of glutathione, leading to the signs and symptoms of glutathione synthetase deficiency.



The GSS gene provides instructions for making an enzyme called glutathione synthetase. Glutathione synthetase participates in a process called the gamma-glutamyl cycle. The gamma-glutamyl cycle is a sequence of chemical reactions that takes place in most of the body's cells. These reactions are necessary for the production of glutathione, a small molecule made of three protein building blocks (amino acids). Glutathione protects cells from damage caused by unstable oxygen-containing molecules, which are byproducts of energy production. Glutathione is called an antioxidant because of its role in protecting cells from the damaging effects of these unstable molecules. Glutathione also helps process medications and cancer-causing compounds (carcinogens), and helps build DNA, proteins, and other important cellular components.

Most of the GSS mutations involved in glutathione synthetase deficiency change single amino acids in glutathione synthetase. Other mutations disrupt how genetic information from the GSS gene is pieced together to make a blueprint for producing the enzyme. The altered glutathione synthetase enzyme may be unstable, shorter than usual, or the wrong shape. All of these changes reduce the activity of the enzyme and disrupt the gamma-glutamyl cycle, preventing adequate production of glutathione.


Gene Locations:


Cytogenetic Location: 20q11.22, which is the long (q) arm of chromosome 20 at position 11.22








Molecular Location: base pairs 34,928,433 to 34,956,027 on chromosome 20 (Homo sapiens Annotation Release 108, GRCh38.p7)








Cytogenetic Location: 1p31.1, which is the short (p) arm of chromosome 1 at position 31.1

Molecular Location: base pairs 70,411,218 to 70,441,949 on chromosome 1 (Homo sapiens Annotation Release 108, GRCh38.p7)








CTH gene: This gene encodes a cytoplasmic enzyme in the trans-sulfuration pathway that converts cystathione derived from methionine into cysteine. Glutathione synthesis in the liver is dependent upon the availability of cysteine.







​​Sources:


https://en.wikipedia.org/wiki/Glutathione

https://draxe.com/glutathione/

https://en.wikipedia.org/wiki/Vitamin_D

https://en.wikipedia.org/wiki/Glutathione

​​http://drhyman.com/blog/2010/05/19/glutathione-the-mother-of-all-antioxidants/

https://ghr.nlm.nih.gov/condition/glutathione-synthetase-deficiency#diagnosis

https://ghr.nlm.nih.gov/gene/GSS

https://ghr.nlm.nih.gov/gene/GSS#location

https://www.ncbi.nlm.nih.gov/gene/2937

https://ghr.nlm.nih.gov/chromosome/1

https://ghr.nlm.nih.gov/gene/CTH#location

https://www.ncbi.nlm.nih.gov/gene/1491


* use in moderation and seek health monitor advise. Overdosing can be dangerous to your health