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N-Acetyl Cysteine (NAC)

The amino acid L-cysteine has a derivative called N-acetyl cysteine (NAC). It functions as a strong antioxidant because it is a source of sulfhydryl (-SH) groups in the body. Additionally, glutathione levels in the body are raised by N-acetyl cysteine, and decreased levels of glutathione has been linked to a number of pathologies. 

For decades, nutritional supplements have contained N-acetyl cysteine (NAC).  However, as of 2020, the FDA began to controversially warn businesses that the use of N-acetyl cysteine in supplements was unlawful.

Mechanisms of Action

N-acetyl cysteine, which is transformed into cysteine and then glutathione, may easily pass the cell membrane while glutathione cannot. Hydroxyl-free radicals and hydrogen peroxide are examples of reactive oxygen species (ROS) that lower glutathione concentrations both inside and outside of cells. A particularly effective technique to restore glutathione and lessen ROS damage is with N-acetyl cysteine [x].


N-acetyl cysteine breaks the disulfide bonds in mucus glycoproteins, which makes biofilms unstable [x].

There is evidence from in vitro and animal studies that N-acetyl cysteine has anticancer properties. (X,X,X,X,X,X)

Results from certain in vitro and animal studies indicate that N-acetyl cysteine reduces the invasiveness and angiogenesis of tumor cells, albeit the exact anticancer mechanism is yet unknown (x). 

N-acetyl cysteine may stimulate anti-angiogenesis through the formation of angiostatin, which encourages vascular collapse of the tumor, according to other animal models (X). 

Other animal studies indicate that alterations in the processing of TNF-alpha and TNF receptors are associated with the anticancer effect of N-acetyl cysteine (X). 

N-acetyl cysteine may prevent the growth of hormone-independent prostate cancer cell lines through anti-NF-kappaB action, according to certain in vitro research (X). Other in vitro studies show that the anticancer effects of N-acetyl cysteine may be explained by increased adherence of tumor cells to peripheral blood mononuclear cells (X) or by inhibiting the synthesis of VEGF (vascular endothelial growth factor) (X).

Neurotransmitter Systems 


The most prevalent excitatory neurotransmitter in the central nervous system (CNS) is glutamate, which is essential for many different CNS processes. Up to 70–80% of all synapses in the CNS are thought to use glutamate for intercellular communication [x,x].   

Glutamatergic transmission in the central nervous system (CNS) is impacted by NAC through a multistep indirect process. Following NAC’s biotransformation into cysteine, cystine enters glial cells in a 1:1 stoichiometry with glutamate trafficking into the extracellular space.

NAC can thereby increase extracellular glutamate levels and inhibit neuronal release of synaptic glutamate under conditions of dysregulated glutamate signaling, such as when extracellular glutamate levels are low. 

Thus, NAC regulates glial-glutamate transporters,  modulates glutamatergic dysfunction [x] , and protects neuronal cells from glutamate-induced excitotoxicity [x]. 


Dopamine is a catecholamine that is produced naturally and is obtained from the amino acid tyrosine through the decarboxylation of dihydroxyphenylalanine (l-DOPA). Dopamine is a precursor to epinephrine and norepinephrine.

Dopamine is a primary transmitter in the basal ganglia, and plays a key role in controlling movement.  Memory, attention, and cognition issues can be caused by abnormal dopaminergic transmission, which is also linked to schizophrenia and psychotic diseases. Parkinson’s and Alzheimer’s diseases are linked to the degeneration of dopaminergic neurons.

Dopamine can be changed into other substances by reactive oxygen species such as dopamine quinones or dopaminochrome, which are linked to cytotoxicity and apoptosis. Despite having a low reactive oxygen species (ROS) reactivity, N-acetylcysteine is still a widely utilized antioxidant [x], potentially owing to its ability to increase glutathione which is a major ROS scavenger reducing oxidative stress[x]. 

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