Evidence map›Paper›PMID 27043646›Full record

ArticleBiomolecules2016

The Involvement of Acetaldehyde in Ethanol-Induced Cell Cycle Impairment.

Marc A Scheer, Katrina J Schneider, Rochelle L Finnigan, Eamon P Maloney, Mark A Wells, Dahn L Clemens

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Selective Killing of Cancer Cells by Nonplanar Aromatic Hydrocarbon-Induced DNA Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019
    Article
  6. Review
  7. Review
  8. 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

6 authors at 1 institution in 1 country.

Marc A ScheerDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. Scheer77@aol.com.
Katrina J SchneiderDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. km0308@hotmail.com.
Rochelle L FinniganDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. rochelle.finnigan@yahoo.com.
Eamon P MaloneyDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. epmaloney@gmail.com.
Mark A WellsDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. wellsma@gmail.com.
Dahn L ClemensDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA. dclemens@unmc.edu.
University of Nebraska Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocytes metabolize the vast majority of ingested ethanol. This metabolic activity results in hepatic toxicity and impairs the ability of hepatocytes to replicate. Previous work by our group has shown that ethanol metabolism results in a G2/M cell cycle arrest. The intent of these studies was to discern the roles of acetaldehyde and reactive oxygen, two of the major by-products of ethanol metabolism, in the G2/M cell cycle arrest.

methodsTo investigate the role of ethanol metabolites in the cell cycle arrest, VA-13 and VL-17A cells were used. These are recombinant Hep G2 cells that express alcohol dehydrogenase or alcohol dehydrogenase and cytochrome P450 2E1, respectively. Cells were cultured with or without ethanol, lacking or containing the antioxidants N-acetylcysteine (NAC) or trolox, for three days. Cellular accumulation was monitored by the DNA content of the cultures. The accumulation of the cyclin-dependent kinase, Cdc2 in the inactive phosphorylated form (p-Cdc2) and the cyclin-dependent kinase inhibitor p21 were determined by immunoblot analysis.

resultsCultures maintained in the presence of ethanol demonstrated a G2/M cell cycle arrest that was associated with a reduction in DNA content and increased levels of p-Cdc2 and p21, compared with cells cultured in its absence. Inclusion of antioxidants in the ethanol containing media was unable to rescue the cells from the cell cycle arrest or these ethanol metabolism-mediated effects. Additionally, culturing the cells in the presence of acetaldehyde alone resulted in increased levels of p-Cdc2 and p21.

conclusionsAcetaldehyde produced during ethanol oxidation has a major role in the ethanol metabolism-mediated G2/M cell cycle arrest, and the concurrent accumulation of p21 and p-Cdc2. Although reactive oxygen species are thought to have a significant role in ethanol-induced hepatocellular damage, they may have a less important role in the inability of hepatocytes to replace dead or damaged cells.

Indexed as

AcetaldehydeAcetylcysteineAlcohol DehydrogenaseAntioxidantsCDC2 Protein KinaseCell LineChromansCyclin-Dependent Kinase Inhibitor p21EthanolG2 Phase Cell Cycle CheckpointsHep G2 CellsHumansImmunoblottingM Phase Cell Cycle CheckpointsPhosphorylationReactive Oxygen Species6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acidAcetaldehydeAcetylcysteineAlcohol DehydrogenaseAntioxidantsCDC2 Protein KinaseChromansCyclin-Dependent Kinase Inhibitor p21EthanolReactive Oxygen Speciesacetaldehydecell cycle arrestcyclin-dependent kinase inhibitorscyclin-dependent kinasesethanol metabolism

Identifiers

PMID27043646
PMCPMC4919912
OpenAlexW2312542899

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.