Glutathione Injections CAS 70-18-8 L-Glutathione reduced Glutathione

Description:

Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool.

Use

Glutathione supplementation has been evaluated in clinical trials in various formulations (eg, oral, intravenous [IV], topical, intranasal, nebulized) for its effects on HIV, Parkinson disease, Alzheimer disease, autism, cystic fibrosis, and cardiovascular diseases, among other conditions. N-acetylcysteine, as the precursor to glutathione, has demonstrated efficacy in raising glutathione levels and is frequently chosen for this purpose.

Dosing

Glutathione has been evaluated in clinical trials in various formulations, including oral, IV, topical, intranasal, and nebulized. The oral formulation has shown mixed results, with some data suggesting it does not increase RBC glutathione and other data showing efficacy. Liposomal formulations of glutathione may confer better effects, but further research is needed. N-acetylcysteine, as the precursor to glutathione, has demonstrated efficacy in raising glutathione levels. Cystic fibrosis: In a clinical trial of children with cystic fibrosis, oral reduced glutathione 65 mg/kg/day (divided into 3 doses per day at mealtimes) was administered for 6 months. Parkinson disease: A small clinical study used IV glutathione at a dosage of 1,400 mg 3 times per week for 4 weeks.

Appearance: Powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: To be determined

Shelf Life: >2 years if stored properly

Drug Formulation: To be determined

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

  Why choose us