Alpha Lipoic Acid
Lipoic acid is both a water and fat-soluble antioxidant with the reduced form dihydrolipoic acid (DHLA) having even more antioxidant activity. Lipoic acid is found in cellular mitochondria and plays a role in energy production.
Functions of Lipoic acid:
• ALA is an antioxidant capable of quenching various reactive oxygen species
• As a chelator, ALA can trap metals in the blood circulation preventing cellular damage
• ALA can enter nerve tissue and prevent glucose-related oxidative damage
• Can regenerate reduced glutathione
• Can recycle reduced vitamin C and indirectly participate in the regeneration of vitamin E
• Has a role in energy production (ATP synthesis)
• Is a cofactor of alpha-keto-dehydrogenase
• Lipoic acid is bound to protein and is a cofactor in oxidative decarboxylation
ALA is easily absorbed and transported across cell membranes; thus, free radical protection occurs both inside and outside of cells. It is water- and fat-soluble, which makes it more effective against a broader range of free radicals than vitamin C (water-soluble) and vitamin E (fat-soluble) alone. ALA administration also increases intracellular levels of glutathione, the animal body’s most important antioxidant.
The body routinely converts ALA to DHLA, a more effective antioxidant. Both forms can quench peroxynitrite radicals, which are responsible in part for heart, lung, and neurological disease, as well as for inflammation. In oxidative stress models, such as ischemia, reperfusion injury, and radiation injury, ALA was shown to be beneficial.
ALA has been shown to be beneficial in types 1 and 2 diabetes, preventing various pathologies associated with the disease, such as reperfusion injury, macular degeneration, cataracts, and neuropathy. The overproduction of reactive oxygen species in mitochondria induced by hyperglycemia is central to the pathogenesis of endothelial damage in diabetes.
Under physiological conditions, metal ions such as iron, copper, and zinc are important and necessary cofactors for normal function of many proteins. Transition metal deficiency or excess can lead to or affect the progression of many diseases. Both ALA and DHLA have been shown to chelate metal ions by forming stable complexes with the ions. Consequently, ALA may have therapeutic potential in transition metal-mediated cellular toxicity. In addition, LA and DHLA contribute to heavy metal detoxification.
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