Potential Role Of N-acetylcysteine Research Articles

The protective effect of N-acetylcysteine on hippocampal ferroptosis in an experimental obesity model

Ferroptosis is a non-apoptotic cell death closely related to a metabolic pathway involving iron overload, imbalanced glutathione metabolism, oxidative stress and lipid peroxidation damage. Obesity is closely associated with these imbalances. In this study, we aimed to investigate the effect of hippocampal ferroptosis in an obesity model and the potential role of N-acetylcysteine (NAC) against ferroptosis. A high-fat (60%) dietary pattern was used to establish an obesity model for 15 weeks. NAC was administered to NAC and Obese+NAC (ObNAC) groups by oral gavage at a dose of 150 mg/kg for 3 weeks. Glutathione peroxidase 4 (GPX4) and the cystine transporter solute carrier family 7- member 11 (SLC7A11) expression levels were investigated immunohistochemically to detect ferroptosis in hippocampal tissues. In the statistical analysis, H-scores of GPX4 and SLC7A11 in the hippocampus sections of the Ob group were significantly lower than in the control, NAC and ObNAC groups (p

The Potential Role for N-Acetylcysteine in Improving Procurement and Preservation Strategies in Liver Transplantation-A Commentary.

The Potential Role for N-Acetylcysteine in Improving Procurement and Preservation Strategies in Liver Transplantation-A Commentary.

Potential role of N-acetylcysteine on chlorpyrifos-induced neurotoxicity in rats.

Chlorpyrifos (CPF) is a widely used organophosphate insecticide with several harmful effects. N-acetylcysteine (NAC) represents an ideal antixenobiotic; it can directly enter endogenous biochemical processes and is used as adjunctive treatment for psychiatric disorders. We aimed to evaluate the neuroprotective effect of NAC as an antioxidant drug against CPF-induced neurotoxicity in adult male albino rat brains. Twenty-eight male Wister rats were allocated into four groups (n = 7) and were administered the following for 28 days: group I (control group), physiological saline (0.9% NaCl); group II (CPF group), 10 mg/kg body weight (BW) CPF; group III (NAC group), 100 mg/kg BW NAC; and group VI (CPF+NAC group), NAC 1 h before CPF. CPF intoxication resulted in acetylcholinesterase inhibition, reduced glutathione content, and elevated levels of malondialdehyde and nitric oxide, which are oxidative stress biomarkers. CPF also depleted the activity of antioxidant enzymes, superoxide dismutase and catalase, and levels of inflammatory mediators, tumor necrosis factor-α, interleukin (IL)-6, and IL-1β. Levels of vascular endothelial growth factor, Bax, and the proapoptotic caspases-3 also increased, while brain-derived neurotrophic factor level decreased. Additionally, CPF significantly diminished Bcl-2 (an antiapoptotic protein) in rat brain cortical tissue. NAC treatment was found to protect brain tissue by reversing the CPF-induced neurotoxicity. Our results show the antioxidant, antiinflammatory, and antiapoptotic effects of NAC on CPF-induced neurotoxicity in rat brain tissue.

A potential role for N-acetylcysteine in the management of methamphetamine dependence.

Methamphetamine dependence is a growing problem in Australia and globally. Currently, there are no approved pharmacotherapy options for the management of methamphetamine dependence. N-acetylcysteine is one potential pharmacotherapy option. It has received growing attention as a therapy for managing addictions because of its capacity to restore homeostasis to brain glutamate systems disrupted in addiction and thereby reduce craving and the risk of relapse. N-acetylcysteine also has antioxidant properties that protect against methamphetamine-induced toxicity and it may therefore assist in the management of the neuropsychiatric and neurocognitive effects of methamphetamine. This commentary overviews the actions of N-acetylcysteine and evidence for its efficacy in treating addiction with a particular focus on its potential utility for methamphetamine dependence. We conclude that the preliminary evidence indicates a need for full-scale trials to definitively establish whether N-acetylcysteine has a therapeutic benefit and the nature of this benefit, for managing methamphetamine dependence. [McKetin R, Dean O, Baker A. L, Carter G, Turner A, Kelly P. J, Berk M. A potential role for N-acetylcysteine in the management of methamphetamine dependence. Drug Alcohol Rev 2017;36:153-159].

Potential Role of N-Acetylcysteine in the Management of Substance Use Disorders

There is a clear and pressing need to expand pharmacotherapy options for substance use disorders (SUDs) in order to improve sustained abstinence outcomes. Preclinical literature has demonstrated the role of glutamate in addiction, suggesting that new targets for pharmacotherapy should focus on the restoration of glutamatergic function. Glutamatergic agents for SUDs may span multiple addictive behaviors and help demonstrate potentially overlapping mechanisms in addiction. The current review will focus specifically on N-acetylcysteine (NAC), a safe and well-tolerated glutamatergic agent, as a promising potential pharmacotherapy for the treatment of SUDs across several substances of abuse. Building on recently published reviews of the clinical efficacy of NAC across a broad range of conditions, this review will more specifically discuss NAC as a pharmacotherapy for SUDs, devoting particular attention to the safety and tolerability profile of NAC, the wealth of preclinical evidence that has demonstrated the role of glutamate dysregulation in addiction, and the limited but growing clinical literature that has assessed the efficacy of NAC across multiple substances of abuse. Preliminary clinical studies show the promise of NAC in terms of safety, tolerability, and potential efficacy for promoting abstinence from cocaine, nicotine, and cannabis. Results from randomized clinical trials have been mixed, but several mechanistic and methodological factors are discussed to refine the use of NAC in promoting abstinence and relapse prevention across several substances of abuse. Further preclinical and clinical investigation into the use of NAC for SUDs will be vital in addressing current deficits in the treatment of SUDs.