Evidence map›Paper›PMID 28599714›Full record

ArticleAlcohol (Fayetteville, N.Y.)2017

Effects of moderate alcohol consumption on gene expression related to colonic inflammation and antioxidant enzymes in rats.

DawnKylee S Klarich, Jerrold Penprase, Patricia Cintora, Octavio Medrano, Danielle Erwin, Susan M Brasser, Mee Young Hong

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Beyond GWAS of Colorectal Cancer: Evidence of Interaction with Alcohol Consumption and Putative Causal Variant for the 10q24.2 Region.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. 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

7 authors at 1 institution in 1 country.

DawnKylee S KlarichSchool of Exercise and Nutritional Sciences, San Diego State University, San Diego, CA, USA.
Jerrold PenpraseDepartment of Psychology, San Diego State University, San Diego, CA, USA.
Patricia CintoraDepartment of Psychology, San Diego State University, San Diego, CA, USA.
Octavio MedranoDepartment of Psychology, San Diego State University, San Diego, CA, USA.
Danielle ErwinDepartment of Psychology, San Diego State University, San Diego, CA, USA.
Susan M BrasserDepartment of Psychology, San Diego State University, San Diego, CA, USA.
Mee Young HongSchool of Exercise and Nutritional Sciences, San Diego State University, San Diego, CA, USA. Electronic address: mhong2@mail.sdsu.edu.
San Diego State University · US

Funding

Insular Cortical Processing in Alcohol AddictionR21AA023291 · NIAAA · SAN DIEGO STATE UNIVERSITY · PI BRASSER, SUSAN M · 2014 to 2015
$388k
NIAAA NIH HHS R21 AA023291
6 · The paper itself

Abstract

Excessive alcohol consumption is a risk factor associated with colorectal cancer; however, some studies have reported that moderate alcohol consumption may not contribute additional risk for developing colorectal cancer while others suggest that moderate alcohol consumption provides a protective effect that reduces colorectal cancer risk. The purpose of this study was to determine the effects of moderate voluntary alcohol (20% ethanol) intake on alternate days for 3 months in outbred Wistar rats on risk factors associated with colorectal cancer development. Colonic gene expression of cyclooxygenase-2, RelA, 8-oxoguanine DNA glycosylase 1, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase M1, and aldehyde dehydrogenase 2 were determined. Blood alcohol content, liver function enzyme activities, and 8-oxo-deoxyguanosine DNA adducts were also assessed. Alcohol-treated rats were found to have significantly lower 8-oxo-deoxyguanosine levels in blood, a marker of DNA damage. Alanine aminotransferase and lactate dehydrogenase were both significantly lower in the alcohol group. Moderate alcohol significantly decreased cyclooxygenase-2 gene expression, an inflammatory marker associated with colorectal cancer risk. The alcohol group had significantly increased glutathione-S-transferase M1 expression, an antioxidant enzyme that helps detoxify carcinogens, such as acetaldehyde, and significantly increased aldehyde dehydrogenase 2 expression, which allows for greater acetaldehyde clearance. Increased expression of glutathione-S-transferase M1 and aldehyde dehydrogenase 2 likely contributed to reduce mucosal damage that is caused by acetaldehyde accumulation. These results indicate that moderate alcohol may reduce the risk for colorectal cancer development, which was evidenced by reduced inflammation activity and lower DNA damage after alcohol exposure.

Indexed as

Alcohol Drinking8-Hydroxy-2'-DeoxyguanosineAldehyde Dehydrogenase, MitochondrialAnimalsAntioxidantsColitisColorectal NeoplasmsCyclooxygenase 2DeoxyguanosineDNA DamageEthanolGene ExpressionGlutathione TransferaseInflammationLiverMale8-Hydroxy-2'-DeoxyguanosineAldehyde Dehydrogenase, MitochondrialAldh2 protein, ratAntioxidantsCyclooxygenase 2DeoxyguanosineEthanolGlutathione TransferaseAlcoholColorectal cancerDNA damageInflammationModerate

Identifiers

PMID28599714
PMCPMC5512456
OpenAlexW2605441142

What OpenQuestion holds

Textmetadata
LicenceTDM
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.