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. 2021 Aug 11;19(8):1202–1224. doi: 10.2174/1570159X19666201230144109

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© 2021 Bentham Science Publishers

This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

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Fig. (2) — Proposed pathophysiologic targets of N-acetylcysteine (NAC). The various mechanisms by which NAC acts as a neurotransmitter, modulates redox reactions, promotes neurogenesis, corrects mitochondrial dysfunction, and dampens the inflammatory response are described in the text.

Adapted from Berk M, et al. Trends. Pharmacol. Sci., 2013, 34(3), 167-177. ^® Elsevier Inc.

AMPA, 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate; BDNF, brain-derived neurotrophic factor; Bcl-2, B cell lymphoma 2; Ca, calcium; Cys, cysteine; DA, dopamine; Glu, glutamate; Gly, glycine; GSH, glutathione; IL, interleukin; NAC, N-acetylcysteine; NMDA, N-methyl-D-aspartate; NO, nitrous oxide; ROS, reactive oxygen species; TNF, tumor necrosis factor. (A higher resolution / colour version of this figure is available in the electronic copy of the article).