N-acetyl cysteine in the treatment of cannabis use disorder: A systematic review of clinical trials

Sharma, Rishi; Tikka, Sai Krishna; Bhute, Ashish Ramesh; Bastia, Binaya Kumar

doi:10.1016/j.addbeh.2022.107283

Cited by 7 publications

(4 citation statements)

References 45 publications

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“…Rare cases of hepatotoxicity Max 0.5 mg/day in ESRD; be mindful considering the risk of hepatorenal syndrome [26] Bupropion Start: 150 mg sustained release daily Maintenance: 150 mg twice daily Duration: 12 wk -FDA-approved second line for smoking cessation [24] -Start 1 week before target quit date -Typical duration of treatment is 12 wk, but use of up to 1 year has been shown to reduce relapse Rare cases of hepatotoxicity Consider dose reduction in moderatesevere renal impairment and severe hepatic impairment [27] Naltrexone Start: 12.5 mg PO Maintenance: 50 PO mg -Non-FDA approved -Evidence of improved quit rates and decreased cravings [28] -Start 1 week before target quit date Rare potential for hepatoxicity; black box warning for liver disease removed [29] Be mindful of interactions with opioids. Nortriptyline 75-100 mg/day -Non-FDA approved -Six placebo-controlled trials have shown nortriptyline efficacy in quit rates [30] Caution in severe liver disease due to considerable anticholinergic side effects Clonidine 0.1-0.5 mg/day -Non-FDA approved -Poor quality trial associated with a slight increase in smoking cessation in oral and transdermal formulations [31] No evidence of hepatoxicity Cannabis cessation NAC 2400 mg/day -Non-FDA approved -Some evidence for promoting abstinence and reduced cravings -Studies show mixed results and larger-scale studies are required to demonstrate efficacy [32] No evidence of hepatotoxicity Gabapentin 1200 mg/day -Non-FDA approved -Double-blind RCT with evidence of decreased withdrawals and cannabis use [33] Use with caution in hepatic encephalopathy due to sedative effects.…”

Section: Mixed Evidencementioning

confidence: 99%

“…The endogenous cannabinoid network in the liver becomes upregulated in CLD. Emerging evidence highlights the role of an active endogenous cannabinoid system in liver pathology 32 . The effects of CBD and THC on this network, however, are nuanced and contradictory; evidence suggests both protective and toxic effects on liver pathology (Table 1).…”

Section: Introductionmentioning

confidence: 99%

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Tobacco, cannabis, and the liver

Tareen,

Winder

2024

Clinical Liver Disease

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Section: Mixed Evidencementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tobacco, cannabis, and the liver

Tareen,

Winder

2024

Clinical Liver Disease

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“…N-acetylcysteine (NAC) is sulfhydryl compound which is the acetylated amino acid L-cysteine (Mohamed et al, 2022). It possesses multiple biological influences including respiratory tract (Guerini et al, 2022), neurodegenerative (Sharma et al, 2022), renal (Nejati et al, 2022) and cardiac disorders . This study emphasizes the theory of protective effect of NAC on liver injury ISSN (Print) 2786-0272 ISSN (Online) 2786-0280…”

Section: Introductionmentioning

confidence: 99%

N-Acetyl cysteine alleviates carbon-tetrachloride induced acute liver injury in rats

Mansour

El‐Zeftawy

Aboubakr

et al. 2022

New Valley Veterinary Journal

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The liver is a vital organ that performs most of the body's metabolic and detoxifying functions. There are various exogenous and endogenous factors that might cause liver issues. Carbon tetrachloride (CCL4) is non-inflammable colorless organic compound and employed in a variety of industrial fields. N-acetylcysteine (NAC) is one of the prospective pharmaceutical candidates possesses multiple clinical applications. The purpose of this study is to determine whether NAC has a protective effect in cases of liver injury or not. Thirty male albino rats were involved in the study, which lasted one month. They were categorized into three groups: control, liver injury group (0.5 ml/kg rat body weight (Bwt) CCL4 administered orally twice a week), and protective group (150 mg/kg Bwt NAC supplied orally). Serum lipid and protein profiles and liver enzymes activities were evaluated. Antioxidant, oxidative stress, and anti-inflammatory parameters were also assessed. Additionally, hepatic tissue was subjected to a histopathological investigation. The biochemical and histopathological results revealed dramatic improvement of studied parameters in NAC protective group comparing to liver injury one. Hence, we can conclude that, NAC shown a great potential in attenuating liver injury induced by CCL4 via refinement tumor necrosis factor-alpha, interleukin-6 and reduced glutathione pathway.

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“…N-acetyl cysteine (NAC) is a precursor of glutathione that can directly scour oxygen free radicals and reduce production of ROS (Diao et al, 2020; Sharma et al, 2022). However, it is not clear whether NAC can reduce aniline-induced liver injury via reduced production of ROS.…”

Section: Introductionmentioning

confidence: 99%

Aniline exposure activates receptor-interacting serine/threonineprotein kinase 1 and causes necroptosis of AML12 cells

Jin

Zhang

et al. 2022

Toxicol Ind Health

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With the increased use of aniline, potential impacts on human health cannot be ignored. The hepatotoxicity of aniline is largely unknown and the underlying mechanism remains unclear. Therefore, the aim of the present study was to investigate the hepatotoxicity of aniline and elucidate the underlying mechanism. AML12 cells were exposed to different concentrations of aniline (0, 5, 10, or 20 mM) to observe changes to reactive oxygen species (ROS) production and the expression patterns of necroptosis-related proteins (RIPK1, RIPK3, and MLKL). The potential mechanism underlying aniline-induced hepatotoxicity was explored by knockout of RIPK1. The results showed that aniline induced cytotoxicity in AML12 cells in a dose-dependent manner in addition to the production of ROS and subsequent necroptosis of AML12 cells. Silencing of RIPK1 reversed upregulation of necroptosis-related proteins in AML12 cells exposed to aniline, demonstrating that aniline-induced ROS production was related to necroptosis of AML12. Moreover, aniline promoted intracellular RIPK1 activation, suggesting that the RIPK1/ROS pathway plays an important role in aniline-induced hepatotoxicity. NAC could quench ROS and inhibit necroptosis. These results provide a scientific basis for future studies of aniline-induced hepatotoxicity for the prevention and treatment of aniline-induced cytotoxicity.

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N-acetyl cysteine in the treatment of cannabis use disorder: A systematic review of clinical trials

Cited by 7 publications

References 45 publications

Tobacco, cannabis, and the liver

Tobacco, cannabis, and the liver

N-Acetyl cysteine alleviates carbon-tetrachloride induced acute liver injury in rats

Aniline exposure activates receptor-interacting serine/threonineprotein kinase 1 and causes necroptosis of AML12 cells

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