Evidence map›Paper›PMID 18499779›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2008

Intermittent hypoxia conditioning prevents behavioral deficit and brain oxidative stress in ethanol-withdrawn rats.

Marianna E Jung, James W Simpkins, Andrew M Wilson, H Fred Downey, Robert T Mallet

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Cardioprotection by intermittent hypoxia conditioning: evidence, mechanisms, and therapeutic potential.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  10. Intermittent hypoxia training blunts cerebrocortical presenilin 1 overexpression and amyloid-β accumulation in ethanol-withdrawn rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cellular and mitochondrial effects of alcohol consumption.International journal of environmental research and public health · 2010
    Review
  19. Article
  20. Intermittent Hypoxia Training for Treating Mild Cognitive Impairment: A Pilot Study.American journal of Alzheimer's disease and other dementias
    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

5 authors at 1 institution in 1 country.

Marianna E JungDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA.
James W Simpkins
Andrew M Wilson
H Fred Downey
Robert T Mallet
University of North Texas · US

Funding

Effects of Age on Ethanol Withdrawal Toxicity: Mechanisms and TherapyR01AA015982 · NIAAA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JUNG, MARIANNA E · 2006 to 2010
$1.4M
Estrogens for Alcoholism &Its Neurological ConsequencesR01AA013864 · NIAAA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SIMPKINS, JAMES W. · 2004 to 2008
$1.1M
Cardioprotective Adaptation to Intermittent HypoxiaR21AT003598 · NCCIH · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI MALLET, ROBERT T · 2007 to 2008
$392k
NCCIH NIH HHS AT003598NIAAA NIH HHS AA013864NIAAA NIH HHS AA015982
6 · The paper itself

Abstract

Intermittent hypoxia (IH) has been found to protect brain from ischemic injury. We investigated whether IH mitigates brain oxidative stress and behavioral deficits in rats subjected to ethanol intoxication and abrupt ethanol withdrawal (EW). The effects of IH on overt EW behavioral signs, superoxide generation, protein oxidation, and mitochondrial permeability transition pore (PTP) opening were examined. Male rats consumed dextrin or 6.5% (wt/vol) ethanol for 35 days. During the last 20 days, rats were treated with repetitive (5-8 per day), brief (5-10 min) cycles of hypoxia (9.5-10% inspired O2) separated by 4-min normoxia exposures. Cerebellum, cortex, and hippocampus were biopsied on day 35 of the diet or at 24 h of EW. Superoxide and protein carbonyl contents in tissue homogenates and absorbance decline at 540 nm in mitochondrial suspensions served as indicators of oxidative stress, protein oxidation, and PTP opening, respectively. Although IH altered neither ethanol consumption nor blood ethanol concentration, it sharply lowered the severity of EW signs including tremor, tail rigidity, and startle response. Compared with dextrin and ethanol per se, in the three brain regions, EW increased superoxide and protein carbonyl contents and accelerated PTP opening in a manner ameliorated by IH. Administration of antioxidant N-acetylcysteine throughout the IH program abrogated the reductions in EW signs and superoxide content, implicating IH-induced ROS as mediators of the salutary adaptations. We conclude that IH conditioning during chronic ethanol consumption attenuates oxidative damage to the brain and mitigates behavioral abnormalities during subsequent EW. IH-induced ROS may evoke this powerful protection.

Indexed as

Ischemic PreconditioningAcetylcysteineAnimalsAntioxidantsBehavior, AnimalBrain ChemistryCentral Nervous System DepressantsDextrinsDietEthanolHypoxiaMaleMitochondriaMitochondrial MembranesMitochondrial SwellingOxidantsAcetylcysteineAntioxidantsCentral Nervous System DepressantsDextrinsEthanolOxidantsSuperoxides

Identifiers

PMID18499779
PMCPMC2519950
OpenAlexW2153089178

What OpenQuestion holds

Textmetadata
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.