Evidence map›Paper›PMID 24299490›Full record

ArticleNeuropathology and applied neurobiology2014

N-acetyl-L-cysteine protects against cadmium-induced neuronal apoptosis by inhibiting ROS-dependent activation of Akt/mTOR pathway in mouse brain.

Sujuan Chen, Qian Ren, Jinfei Zhang, Yangjing Ye, Zhen Zhang, Yijiao Xu, Min Guo, Haiyan Ji, Chong Xu, Chenjian Gu and 3 more

Open access · greenAbstract read
In one paragraph

Article in Neuropathology and applied neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 113 citations in OpenAlex.

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  8. A soybean based-diet prevents Cadmium access to rat cerebellum, maintaining trace elements homeostasis and avoiding morphological alterations.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Sujuan ChenJiangsu Key Laboratory for Microbes and Functional Genomics, Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing, China.
Qian Ren
Jinfei Zhang
Yangjing Ye
Zhen Zhang
Yijiao Xu
Min Guo
Haiyan Ji
Chong Xu
Chenjian Gu
Wei Gao
Shile Huang
Long Chen
Nanjing Normal University · CNLouisiana State University Health Sciences Center Shreveport · US

Funding

mTOR Signaling in Tumor Cell MotilityR01CA115414 · NCI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI HUANG, SHILE · 2006 to 2009
$811k
NCI NIH HHS CA115414NCI NIH HHS R01 CA115414
6 · The paper itself

Abstract

aimsThis study explores the neuroprotective effects and mechanisms of N-acetyl-L-cysteine (NAC) in mice exposed to cadmium (Cd).

methodsNAC (150 mg/kg) was intraperitoneally administered to mice exposed to Cd (10-50 mg/L) in drinking water for 6 weeks. The changes of cell damage and death, reactive oxygen species (ROS), antioxidant enzymes, as well as Akt/mammalian target of rapamycin (mTOR) signalling pathway in brain neurones were assessed. To verify the role of mTOR activation in Cd-induced neurotoxicity, mice also received a subacute regimen of intraperitoneally administered Cd (1 mg/kg) with/without rapamycin (7.5 mg/kg) for 11 days.

resultsChronic exposure of mice to Cd induced brain damage or neuronal cell death, due to ROS induction. Co-administration of NAC significantly reduced Cd levels in the plasma and brain of the animals. NAC prevented Cd-induced ROS and significantly attenuated Cd-induced brain damage or neuronal cell death. The protective effect of NAC was mediated, at least partially, by elevating the activities of Cu/Zn-superoxide dismutase, catalase and glutathione peroxidase, as well as the level of glutathione in the brain. Furthermore, Cd-induced activation of Akt/mTOR pathway in the brain was also inhibited by NAC. Rapamycin in vitro and in vivo protected against Cd-induced neurotoxicity.

conclusionsNAC protects against Cd-induced neuronal apoptosis in mouse brain partially by inhibiting ROS-dependent activation of Akt/mTOR pathway. The findings highlight that NAC may be exploited for prevention and treatment of Cd-induced neurodegenerative diseases.

Indexed as

AcetylcysteineAnimalsApoptosisBrainCadmiumMaleMiceMice, Inbred ICRNeuronsNeuroprotective AgentsOxidative StressProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionTOR Serine-Threonine KinasesAcetylcysteineCadmiummTOR protein, mouseNeuroprotective AgentsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine Kinasescadmiummammalian target of rapamycinN-acetyl-L-cysteineneuronal apoptosisreactive oxygen species

Identifiers

PMID24299490
PMCPMC4043941
OpenAlexW1608663004

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.