The acetyl group (-CH₂CHOOH) differentiates NAC from its dietary precursor cysteine (Figure 1). Addition of this acetyl group to the amino group of cysteine makes the molecule more stable against oxidation than cysteine alone and more bioavailable. ^(9,44) As a source of sulfhydryl (-SH) groups, NAC is converted in the body into metabolites capable of stimulating glutathione (GSH) synthesis, promoting detoxification, and acting directly as a free radical scavenger. ^(5,46) Unlike cysteine, NAC is not found in foods but serves as a delivery form of cysteine. A significant point about research into NAC and cysteine deficiency is that NAC is the agent used and not cysteine or high-cysteine containing proteins such as whey. It is not known whether the same results could be achieved with the use of cysteine or any form of whey protein.

In the treatment of acetaminophen overdose, NAC (Fluimucil^®) is given orally over 18 days or over shorter periods by slow IV infusion. ^(30,33,50) When given within eight hours of acetaminophen ingestion, NAC is protective regardless of the amount of acetaminophen ingested. ⁽⁵¹⁾ NAC (Mucomyst^®) is used in the treatment of respiratory disorders, such as cystic fibrosis and bronchitis, associated with the production of excessive or viscous mucus. ^(13,25,54)

In addition to these established uses, NAC is purported to be useful in colds, liver protection, hepatitis B, chronic bronchitis, acute respiratory distress syndrome, chemotherapy, angina pectoris in combination with conventional therapy, and renal cysteine stones. ^{(1,4,14,15,23,25,48,54,57)}