Evidence map›Paper›PMID 26649137›Full record

ArticleOxidative medicine and cellular longevity2016

Acetaldehyde Induces Cytotoxicity of SH-SY5Y Cells via Inhibition of Akt Activation and Induction of Oxidative Stress.

Tingting Yan, Yan Zhao, Xia Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Impact of Alcohol Consumption on Male Fertility Potential: A Narrative Review.International journal of environmental research and public health · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Neurotoxicity of e-cigarettes.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    Review
  12. Article
  13. Acetaldehyde Induces NeurotoxicityOxidative medicine and cellular longevity · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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

3 authors at 1 institution in 1 country.

Tingting YanDepartment of Bioengineering, Harbin Institute of Technology, Weihai, Shandong 264209, China.
Yan ZhaoDepartment of Bioengineering, Harbin Institute of Technology, Weihai, Shandong 264209, China.
Xia ZhangDepartment of Bioengineering, Harbin Institute of Technology, Weihai, Shandong 264209, China.
Harbin Institute of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. It has been shown that heavy drinking is associated with an earlier onset of neurodegenerative diseases such as Alzheimer's disease. Acetaldehyde, the most toxic metabolite of ethanol, is speculated to mediate the brain tissue damage and cognitive dysfunction induced by the chronic excessive consumption of alcohol. However, the exact mechanisms by which acetaldehyde induces neurotoxicity are not totally understood. In this study, we investigated the cytotoxic effects of acetaldehyde in SH-SY5Y cells and found that acetaldehyde induced apoptosis of SH-SY5Y cells by downregulating the expression of antiapoptotic Bcl-2 and Bcl-xL and upregulating the expression of proapoptotic Bax. Acetaldehyde treatment led to a significant decrease in the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). In addition, acetaldehyde induced the activation of p38 mitogen-activated protein kinase (MAPK) while inhibiting the activation of extracellular signal-regulated kinases (ERKs, p44/p42MAPK). Meanwhile, acetaldehyde treatment caused an increase in the production of reactive oxygen species and elevated the oxidative stress in SH-SY5Y cells. Therefore, acetaldehyde induces cytotoxicity of SH-SY5Y cells via promotion of apoptotic signaling, inhibition of cell survival pathway, and induction of oxidative stress.

Indexed as

AcetaldehydeApoptosisbcl-X ProteinCell Line, TumorCytotoxinsHumansMAP Kinase Signaling SystemOxidative StressProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2AcetaldehydeBCL2L1 protein, humanBCL2 protein, humanbcl-X ProteinCytotoxinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID26649137
PMCPMC4663355
OpenAlexW2229537590

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.