Apart from the polyphenols, other dietary antioxidants have been found to play direct roles in modulating both autophagy and mitophagy. One of the most important of these is alpha lipoic acid.
ALA has been called the 'universal antioxidant': it is readily absorbed from the diet, rapidly converted to its redox couple dihydrolipoic acid (DHLA); it is active in both lipid (membranous) and aqueous (cytoplasmic) phases of the cell. Moreover, both ALA and DHLA have metal chelating activity, allowing them to remove noxious environmental toxins from the body. DHLA acts synergistically with other antioxidants and is capable of regenerating spent antioxidants from their inactive (oxidized) forms. There is substantial recent evidence that ALA affects the expression of regulatory proteins and the genes involved in normal growth and metabolism through various cell signaling mechanisms.
Alpha lipoic acid plays an essential role in supporting mitochondrial health. In its reduced form (DHLA) it reacts with and quenches reactive oxygen species such as the superoxide radical, the hydroxyl radical, hypochlorous acid, peroxyl radicals, and singlet oxygen. ALA also protects cell and organelle membranes by interacting with vitamin C and glutathione, which, in turn, recycle vitamin E. In addition to its antioxidant activities, ALA administration has been shown to prevent the damaging process of glycation (the cross-linking of proteins with sugars).62 In animal-model studies, ALA and acetyl-l-carnitine (ALC), at miniscule concentrations within the cell, can dramatically increase mitochondrial mass, oxygen consumption, and fatty acid oxidation. Acting together, ALA and ALC appear to promote mitochondrial synthesis and enhance cellular metabolism.63
Other very recent investigations highlight the ability of ALA to act as a critical signalling molecule on several fronts: it is capable of up-regulating the synthesis of the cell’s primary endogenous antioxidant glutathione; it induces the activation of the antioxidant nuclear transcription factor Nrf2; it protects mitochondrial function and induces both mitochondrial biogenesis and mitophagy;64-66 and it can temper the activity of the inflammation-promoting nuclear transcription factor NF-kB.
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