Evidence map›Paper›PMID 22403345›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012

Intermittent hypoxia conditioning protects mitochondrial cytochrome c oxidase of rat cerebellum from ethanol withdrawal stress.

Xiaohua Ju, Robert T Mallet, H Fred Downey, Daniel B Metzger, Marianna E Jung

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  12. Intermittent hypoxia training blunts cerebrocortical presenilin 1 overexpression and amyloid-β accumulation in ethanol-withdrawn rats.American journal of physiology.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
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  14. The Role of Presenilin-1 in the Excitotoxicity of Ethanol Withdrawal.The Journal of pharmacology and experimental therapeutics · 2016
    Article
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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

5 authors at 2 institutions in 1 country.

Xiaohua JuDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, Texas 76107-2699, USA.
Robert T Mallet
H Fred Downey
Daniel B Metzger
Marianna E Jung
University of North Texas Health Science Center · USUniversity 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
Intermittent Hypoxia Protects Brain from Ethanol Withdrawal Mechanisms and TherapR21AA018747 · NIAAA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JUNG, MARIANNA E · 2010 to 2011
$392k
NIAAA NIH HHS AA-015982NIAAA NIH HHS AA-018747
6 · The paper itself

Abstract

Intermittent hypoxia (IH) conditioning minimizes neurocognitive impairment and stabilizes brain mitochondrial integrity during ethanol withdrawal (EW) in rats, but the mitoprotective mechanism is unclear. We investigated whether IH conditioning protects a key mitochondrial enzyme, cytochrome c oxidase (COX), from EW stress by inhibiting mitochondrially directed apoptotic pathways involving cytochrome c, Bax, or phosphor-P38 (pP38). Male rats completed two cycles of a 4-wk ethanol diet (6.5%) and 3 wk of EW. An IH program consisting of 5-10 bouts of 5-8 min of mild hypoxia (9.5-10% inspired O(2)) and 4 min of reoxygenation for 20 consecutive days began 3 days before the first EW period. For some animals, vitamin E replaced IH conditioning to test the contributions of antioxidant mechanisms to IH's mitoprotection. During the second EW, cerebellar-related motor function was evaluated by measuring latency of fall from a rotating rod (Rotarod test). After the second EW, COX activity in cerebellar mitochondria was measured by spectrophotometry, and COX, cytochrome c, Bax, and pP38 content were analyzed by immunoblot. Mitochondrial protein oxidation was detected by measuring carbonyl contents and by immunochemistry. Earlier IH conditioning prevented motor impairment, COX inactivation, depletion of COX subunit 4, protein carbonylation, and P38 phosphorylation during EW. IH did not prevent cytochrome c depletion during EW, and Bax content was unaffected by EW ± IH. Vitamin E treatment recapitulated IH protection of COX, and P38 inhibition attenuated protein oxidation during EW. Thus IH protects COX and improves cerebellar function during EW by limiting P38-dependent oxidative damage.

Indexed as

Oxidative StressAlcohol DrinkingAnimalsAntioxidantsApoptosisbcl-2-Associated X ProteinBehavior, AnimalBlotting, WesternCerebellumCytochromes cDisease Models, AnimalElectron Transport Complex IVEthanolHypoxiaImidazolesMaleAntioxidantsBax protein, ratbcl-2-Associated X ProteinCytochromes cElectron Transport Complex IVEthanolImidazolesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsPyridinesSB 203580Vitamin E

Identifiers

PMID22403345
PMCPMC3365408
OpenAlexW2132514466

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.