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66 Nrf2 regulates the expression of ATP-binding cassette transporter B6, inhibits ferroptosis, and slows the development of atherosclerosis

It has been postulated that cysteine may cross the BBB via a sodium-dependent transport system where it is converted into cystine, the di-sulfide derivative of cysteine.51) High levels of cystine stimulate the exchange of intracellular glutamate for cystine through the cystine-glutamate antiporter, thereby elevating non-synaptic glutamate.52,53) This process activates the metabotropic glutamate receptors (mGluR2/3) on presynaptic neurons, responsible for inhibiting the synaptic release of glutamate and thereby restoring extracellular glutamate levels in the nucleus accumbens.54,55) Regulating this exchange system has been shown to improve impulse control and reduce addictive behaviour both pre-clinically and clinically.40,41,56,57) Intracellular cystine can then be reduced back to cysteine and used for GSH production, the potent and most abundant endogenous antioxidant in the body.33,58) A clearer understanding of the pharmacokinetics and pharmacodynamics of NAC has prompted clinical investigations of this nutraceutical as a glutamate-modulating therapeutic agent for psychiatric conditions, including addictive behaviour (such as gambling, cocaine, nicotine and marijuana use),41,59,60) bipolar disorder,61,62) schizophrenia,63,64) and autism.65) The ability of NAC to modulate factors associated with OCD and OCRD, such as the regulation of extracellular glutamate and the reduction of oxidative stress (through direct radical scavenging and increasing GSH activity), indicates that this agent may be an effective treatment for OCD and OCRD.44) Animal studies have provided some support of this hypothesis