Evidence map›Paper›PMID 28062893›Full record

ArticleChild's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery2017

Prenatal alcohol-induced neuroapoptosis in rat brain cerebral cortex: protective effect of folic acid and betaine.

Ibrahim Sogut, Onur Uysal, Aysegul Oglakci, Ferruh Yucel, Kazim Kartkaya, Gungor Kanbak

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Article in Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. DNA Methylation in Alcohol Use Disorder.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Folic acid prevents functional and structural heart defects induced by prenatal ethanol exposure.American journal of physiology. Heart and circulatory physiology · 2021
    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 2 institutions in 1 country.

Ibrahim SogutVocational School of Health Services, Istanbul Bilim University, Yazarlar Sok. No:17, 34394, Istanbul, Turkey. ibrahim.sogut@gmail.com.
Onur UysalVocational School of Health Services, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.
Aysegul OglakciMedical School, Department of Biochemistry, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.
Ferruh YucelMedical School, Department of Anatomy, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.
Kazim KartkayaMedical School, Department of Biochemistry, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.
Gungor KanbakMedical School, Department of Biochemistry, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.
Eskişehir Osmangazi University · TRIstanbul Bilim University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlcohol consumption in pregnancy may cause fetal alcohol syndrome (FAS) in the infant. This study aims to investigate prenatal alcohol exposure related neuroapoptosis on the cerebral cortex tissues of newborn rats and possible neuroprotective effects of betaine, folic acid, and combined therapy.

methodsPregnant rats were divided into five experimental groups: control, ethanol, ethanol + betaine, ethanol + folic acid, and ethanol + betaine + folic acid combined therapy groups. We measured cytochrome c release, caspase-3, calpain and cathepsin B and L. enzyme activities. In order to observe apoptotic cells in the early stages, TUNEL method was chosen together with histologic methods such as assessing the diameters of the apoptotic cells, their distribution in unit volume and volume proportion of cortical intact neuron nuclei.

resultsCalpain, caspase-3 activities, and cytochrome c levels were significantly increased in alcohol group while cathepsin B and L. activities were also found to be elevated albeit not statistically significant. These increases were significantly reversed by folic acid and betaine + folic acid treatments. While ethanol increased the number of apoptotic cells, this increase was prevented in ethanol + betaine and ethanol + betaine + folic acid groups. Morphometric examination showed that the mean diameter of apoptotic cells was increased with ethanol administration while this increase was reduced by betaine and betaine + folic acid treatments.

conclusionWe observed that ethanol is capable of triggering apoptotic cell death in the newborn rat brains. Furthermore, folic acid, betaine, and combined therapy of these supplements may reduce neuroapoptosis related to prenatal alcohol consumption, and might be effective on preventing fetal alcohol syndrome in infants.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsAnimals, NewbornApoptosisBetaineBlood Alcohol ContentCalpainCaspase 3Cathepsin BCathepsin LCentral Nervous System DepressantsCerebral CortexCytochromes cDisease Models, AnimalEthanolFemaleBetaineBlood Alcohol ContentCalpainCaspase 3Cathepsin BCathepsin LCentral Nervous System DepressantsCytochromes cEthanolFolic AcidNeuroprotective AgentsBetaineCalpainCaspase-3Cytochrome cFolic acidNeuroapoptosis

Identifiers

PMID28062893
OpenAlexW2567964136

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Registered trials

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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.