N-Acetyl Cysteine Decreases Mice Brain Acetyl Cholinesterase Activity: An In Vitro Kinetic Study

M, Costa M Costa

doi:10.4172/2329-6674.1000135

Cited by 4 publications

(3 citation statements)

References 28 publications

(32 reference statements)

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“…Treatment with NAC in the present study restored the normal activity of AChE and MAO. NAC has been reported to be an AChE inhibitor 36. The ameliorative effect of NAC may be largely attributed to its antioxidant action and its ability to quench free radicals.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of N-acetylcysteine against cisplatin-induced toxicity in rat brain by modulation of oxidative stress and inflammation

Abdel-Wahab¹,

Moussa²

2019

DDDT

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Background Neurotoxicity is a major obstacle to the effectiveness of cisplatin (CDDP) in cancer chemotherapy. Oxidative stress and inflammation are considered to be the major mechanisms involved in CDDP-induced neurotoxicity. The rationale of our study was to investigate the efficacy of N -acetylcysteine (NAC) at two different doses in the management of CDDP-induced toxicity in rat brain by monitoring its antioxidant and anti-inflammatory effects. Methods Thirty-five male rats were divided into five groups (n=7) as follows: control group (0.5 mL saline), NAC 100 group (100 mg/kg), CDDP group (8 mg/kg), NAC 50 -CDDP group (50 mg/kg NAC and 8 mg/kg CDDP), and NAC 100 -CDDP group (100 mg/kg NAC and 8 mg/kg CDDP). NAC was administered for 20 consecutive days, while CDDP was injected once on day 15 of the treatment protocol. Results The neurotoxicity of CDDP was evidenced by a marked increase in acetylcholinesterase and monoamine oxidase activities. It also induced oxidative stress as indicated by increased levels of lipid peroxidation, nitric oxide, and protein carbonyl with a concomitant decline in reduced glutathione, glutathione peroxidase, glutathione S-transferase, superoxide dismutase, and catalase in the brain. Moreover, CDDP enhanced the synthesis of pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin-1β, and interleukin-6. Treatment with NAC at the two selected doses significantly attenuated CDDP-induced changes in the brain cholinergic function, improved the brain oxidant/antioxidant status, and also reversed the overproduction of pro-inflammatory cytokines in brain and serum. Conclusion NAC could serve as an appropriate and safe complementary therapeutic agent to attenuate the toxicity of CDDP in the brain and therefore improve its outcomes in chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of N-acetylcysteine against cisplatin-induced toxicity in rat brain by modulation of oxidative stress and inflammation

Abdel-Wahab¹,

Moussa²

2019

DDDT

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“…At the time of writing, we are unaware of any previous reports of this finding. However, there is evidence that NAC can increase the contractility of skeletal muscle in other systems ( Okay et al, 2010 ), potentially through inhibition of AChE ( Abdel-Wahab and Moussa, 2019 ; Costa et al, 2015 ). Such inhibition would potentiate cholinergic signals, thereby increasing sensitivity to levamisole.…”

Section: Discussionmentioning

confidence: 99%

Patient-specific variants of NFU1/NFU-1 disrupt cholinergic signaling in a model of multiple mitochondrial dysfunctions syndrome 1

Kropp

Rogers

Kelly

et al. 2023

Disease Models &Amp; Mechanisms

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Neuromuscular dysfunction is a common feature of mitochondrial diseases and frequently presents as ataxia, spasticity, and/or dystonia all of which can severely impact individuals afflicted with mitochondrial diseases. Dystonia is one of the most common symptoms of Multiple Mitochondrial Dysfunctions Syndrome 1, a disease associated with mutations in the causative gene (NFU1) that impairs iron-sulfur cluster biogenesis. We have generated C. elegans strains that recreated patient-specific point variants in the C. elegans ortholog (NFU-1) that result in allele-specific dysfunction. Each of these mutants, Gly147Arg and Gly166Cys, have altered acetylcholine signaling at neuromuscular junctions, but opposite effects on activity and motility. We find that the Gly147Arg variant is hypersensitive to acetylcholine and that knockdown of acetylcholine release rescues nearly all neuromuscular phenotypes of this variant. In contrast, we find that the Gly166Cys variant causes predominantly postsynaptic acetylcholine hypersensitivity due to an unclear mechanism. These results are important for understanding the neuromuscular conditions of MMDS1 patients and potential avenues for therapeutic intervention.

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“…The catalysts hindrance might be fundamentally influenced by pH, in the irreversible no not as much as the reversible case. The rate response of the inhibitor with the catalyst might be influenced by pH on the grounds that the diverse ionic types of the protein may respond at various rates with the inhibitor [26]. Injured movement was higher in the cerebrum of both ordinary and alloxan diabetic rats when contrasted with alternate districts of the notice.…”

Section: Discussionmentioning

confidence: 99%

Anti-Alzheimer Activity of Tacrine Loaded Methoxypoly (Ethylene Glycol) Poly (Caprolactone) Nanoparticles

Joe¹,

Kumar

2018

Asian J Pharm Clin Res

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Objective: The objective of the study was to study the in vitro cytotoxic effects of amyloid-β (Aβ) in SH-SY5Y cells and in vivo therapeutic efficacy of drug-loaded nanoparticles (TMPCN-3) in mice.Methods: In vitro cytotoxic effects of Aβ in SH-SY5Y cells were carried out using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay; cellular uptake study was carried using a laser scanning fluorescence microscope. In vivo therapeutic efficacy of drug loaded nanoparticles, optimized formulation (TMPCN-3) in mice. Animals (n=18) were divided into three different groups each consisting of six animals in each group.Results: Treatment with Aβ-induced cytotoxicity showed a 54% decrease in cell viability. Drug-treated with TMPCN-3 showed greater intracellular accumulation. In the invasive study TMPCN-3 nanoparticles, the SH-SY5Y cells (73%) were decreased when compared to the control cells (91%). In vivo therapeutic efficacy of drug-loaded nanoparticles was studied in mice, Morris water maze task shows polymeric nanoformulations indicates critical change execution (expanded memory maintenance) when contrasted with control, step down condition maintains a considered space from response created by the memory change and polymeric nanoformulations, and after that taken by tacrine and control the quantity of errors are higher. The nanoformulations distributed massive decreasing in acetylcholine esterase level brain homogenate.Conclusion: Tacrine-loaded methoxypoly(ethylene glycol) poly(caprolactone) reveals that the in vitro cell line believes emphasized the reduced risk of tacrine loaded nanoparticles as there is a significant decrease half maximal inhibitory concentration and higher convention of drug in the glial cells and by in vivo reflects was confirmed that nanoformulation indicated improved memory.

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N-Acetyl Cysteine Decreases Mice Brain Acetyl Cholinesterase Activity: An In Vitro Kinetic Study

Cited by 4 publications

References 28 publications

<p>Neuroprotective effect of <em>N</em>-acetylcysteine against cisplatin-induced toxicity in rat brain by modulation of oxidative stress and inflammation</p>

<p>Neuroprotective effect of <em>N</em>-acetylcysteine against cisplatin-induced toxicity in rat brain by modulation of oxidative stress and inflammation</p>

Patient-specific variants of NFU1/NFU-1 disrupt cholinergic signaling in a model of multiple mitochondrial dysfunctions syndrome 1

Anti-Alzheimer Activity of Tacrine Loaded Methoxypoly (Ethylene Glycol) Poly (Caprolactone) Nanoparticles

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