Alpha Lipoic Acid
Alpha Lipoic Acid

What is Alpha-Lipoic Acid?

Alpha lipoic acid is a medium-chain triglyceride found in the liver and yeasts. It functions as a coenzyme in plants, microorganisms and animal tissues. It is important for glucose, carbohydrate, fatty acid, protein and amino acid metabolism.

 

Structure

Molecular Formula: C8H14O2S2

Molecular Weight: 206.3 g/mol

PubChem CID: 864

CAS Number: 1077-28-7

Synonyms: Elemental selenium

MeSH Pharmacological Classification:

Antioxidants: Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues.

ATC Code:

A - Alimentary tract and metabolism

A16 - Other alimentary tract and metabolism products

A16A - Other alimentary tract and metabolism products

A16AX - Various alimentary tract and metabolism products

A16AX01 - Thioctic acid

 

Effects

Alpha lipoic acid neutralizes hydroxyl and singlet oxygen free radicals. It can scavenge reactive oxygen species and reduce other metabolics such as glutathione or vitamins, ensuring that the cellular redox state remains within healthy limits. Thus, it has a protective effect on other antioxidants such as vitamin E, vitamin C, catalase and glutathione. Alpha-lipoic acid (LA) shows a protective effect on oxidative stress-induced apoptosis while it induces apoptosis in various cancer cells. Intracellular Ca(2+) plays a central role in triggering apoptotic pathways. In the present study, we aim to investigate whether LA induces apoptosis in lung cancer cells and whether Ca(2+) is involved in LA-induced apoptosis. We found that LA decreased cell viability and increased DNA fragmentation of the cells. LA activated the caspase-independent pathway, determined by upregulation of poly(ADP-ribose) polymerase (PARP) and increased the nuclear level of apoptosis-inducing factor and caspase-dependent apoptotic pathway, determined by increased levels of cytochrome c and PARP-1 cleavage product. LA-induced apoptotic alterations were inhibited in the cells treated with Ca(2+) chelator BAPTA-AM. In conclusion, LA induces apoptosis through caspase-independent and caspase-dependent pathways, which is mediated by intracellular Ca(2+).