Evidence map›Paper›PMID 28095320›Full record

ArticleFree radical biology & medicine2017

Lethal dysregulation of energy metabolism during embryonic vitamin E deficiency.

Melissa McDougall, Jaewoo Choi, Hye-Kyeong Kim, Gerd Bobe, J Frederik Stevens, Enrique Cadenas, Robert Tanguay, Maret G Traber

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
8.1field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Antioxidants in Personalized Nutrition and Exercise.Advances in nutrition (Bethesda, Md.) · 2018
    Review
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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

8 authors at 3 institutions in 2 countries.

Melissa McDougallLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA; College of Public Health and Human Sciences, Oregon State University, Corvallis, OR 97331, USA.
Jaewoo ChoiLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
Hye-Kyeong KimThe Catholic University of Korea, Seoul, Republic of Korea.
Gerd BobeLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
J Frederik StevensLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA; College of Pharmacy, Oregon State University, Corvallis, OR 97331, USA; Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA.
Enrique CadenasUniversity of Southern California, School of Pharmacy, Los Angeles, CA 90089, USA.
Robert TanguayEnvironmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA; Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA; Sinnhuber Aquatic Research Laboratory, Oregon State University, Corvallis, OR 97331, USA.
Maret G TraberLinus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA; College of Public Health and Human Sciences, Oregon State University, Corvallis, OR 97331, USA; Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA. Electronic address: maret.traber@oregonstate.edu.
Oregon State University · USCatholic University of Korea · KRUniversity of Southern California · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Triple Quadrupole/Linear Ion Trap LC-MS/MS for LPIS10RR027878 · NCRR · OREGON STATE UNIVERSITY · PI STEVENS, JAN FREDERIK · 2010 to 2010
$484k
NCRR NIH HHS S10 RR027878NIEHS NIH HHS P30 ES000210
6 · The paper itself

Abstract

Vitamin E (α-tocopherol, VitE) was discovered in 1922 for its role in preventing embryonic mortality. We investigated the underlying mechanisms causing lethality using targeted metabolomics analyses of zebrafish VitE-deficient embryos over five days of development, which coincided with their increased morbidity and mortality. VitE deficiency resulted in peroxidation of docosahexaenoic acid (DHA), depleting DHA-containing phospholipids, especially phosphatidylcholine, which also caused choline depletion. This increased lipid peroxidation also increased NADPH oxidation, which depleted glucose by shunting it to the pentose phosphate pathway. VitE deficiency was associated with mitochondrial dysfunction with concomitant impairment of energy homeostasis. The observed morbidity and mortality outcomes could be attenuated, but not fully reversed, by glucose injection into VitE-deficient embryos at developmental day one. Thus, embryonic VitE deficiency in vertebrates leads to a metabolic reprogramming that adversely affects methyl donor status and cellular energy homeostasis with lethal outcomes.

Indexed as

Energy MetabolismAnimalsDocosahexaenoic AcidsLipid PeroxidationMitochondriaOxidation-ReductionVitamin EVitamin E DeficiencyZebrafishDocosahexaenoic AcidsVitamin EDocosahexaenoic acidMethyl donorsMitochondriaOxygen consumptionPhosphatidylcholineα-tocopherol

Identifiers

PMID28095320
PMCPMC5344700
OpenAlexW2571676839

What OpenQuestion holds

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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.