Actions of N-Acetylcysteine in the central nervous system: implications for the treatment of neurodegenerative and neuropsychiatric disorders
RIS ID
87288
Abstract
N-Acetylcysteine (NAC) is the N-acetyl derivative of cysteine, and is less reactive, less toxic, and less susceptible to oxidation than cysteine, as well as being more soluble in water. For these reasons it is a better source of cysteine than the parenteral administration of cysteine itself [1]. NAC is rapidly absorbed, with time to peak plasma levels (tmax) being 1.4 ± 0.7 h following oral administration. The average elimination half-life (t112) has been reported to be 2.5 ± 0.6 h [2]. The bioavailability of NAC increases according to the dose, with the peak serum level being on average 16 μmol/L after 600 mg and 35 μmol/L after 1200 mg [3]. When taken orally NAC is readily taken up in the stomach and gut and sent to the liver where it is converted almost entirely to cysteine and used for glutathione (GSH) synthesis [4]. Cysteine that is not converted to GSH is capable of crossing the blood-brain barrier by means of sodium-dependent transport systems [5].
Publication Details
Camfield, D. (2013). Actions of N-Acetylcysteine in the central nervous system: implications for the treatment of neurodegenerative and neuropsychiatric disorders. In C. Stough & A. Scholey (Eds.), Advances in Natural Medicines, Nutraceuticals and Neurocognition (pp. 29-42). United States: CRC Press.