Evidence map›Paper›PMID 32221313›Full record

ArticleScientific reports2020

Mitochondrial dysfunction and DNA damage accompany enhanced levels of formaldehyde in cultured primary human fibroblasts.

Cristina A Nadalutti, Donna F Stefanick, Ming-Lang Zhao, Julie K Horton, Rajendra Prasad, Ashley M Brooks, Jack D Griffith, Samuel H Wilson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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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 2 institutions in 1 country.

Cristina A NadaluttiGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Donna F StefanickGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Ming-Lang ZhaoGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Julie K HortonGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Rajendra PrasadGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Ashley M BrooksCenter for Integrative Bioinformatics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA.
Jack D GriffithLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Samuel H WilsonGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, 27709, USA. wilson5@niehs.nih.gov.
National Institute of Environmental Health Sciences · USUniversity of North Carolina at Chapel Hill · US

Funding

Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Biology of Mammalian Base Excision Repair and HIV-1 ReplicationZIAES050159 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 2009 to 2022
$29.7M
Mechanisms of Nucleic Acid Enzymes - Pol Beta, HIV-1 Reverse Transcriptase and Mammalian Base Repair EnzymesZIAES050158 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 2009 to 2022
$17.0M
HOMOLOOUS RECOMBINATION: ITS MOLECULAR CYTOLOGYR01GM031819 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GRIFFITH, JACK D · 1985 to 2017
$5.2M
BIOLOGY OF MAMMALIAN BASE EXCISION REPAIRZ01ES050159 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 1997 to 2008
$4.5M
Nucleoprotein structures formed at sites of DNA damageR01ES013773 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GRIFFITH, JACK D · 2005 to 2015
$3.2M
Nucleic Acid Enzymes--Pol Beta And Base Repair EnzymesZ01ES050158 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WILSON, SAMUEL H · 1997 to 2008
$2.8M
R-loops at the telomere as a toxic source of genomic instabilityR01ES031635 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GRIFFITH, JACK D · 2020 to 2024
$1.7M
The structure of the telomere as a sentinel of DNA damage.R56ES013773 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GRIFFITH, JACK D · 2019 to 2019
$150k
Intramural NIH HHS Z01 ES050158Intramural NIH HHS Z01 ES050159NCI NIH HHS P01 CA019014NIEHS NIH HHS R01 ES013773NIEHS NIH HHS R01 ES031635NIEHS NIH HHS R56 ES013773NIGMS NIH HHS R01 GM031819
6 · The paper itself

Abstract

Formaldehyde (FA) is a simple biological aldehyde that is produced inside cells by several processes such as demethylation of DNA and proteins, amino acid metabolism, lipid peroxidation and one carbon metabolism (1-C). Although accumulation of excess FA in cells is known to be cytotoxic, it is unknown if an increase in FA level might be associated with mitochondrial dysfunction. We choose to use primary human fibroblasts cells in culture (foreskin, FSK) as a physiological model to gain insight into whether an increase in the level of FA might affect cellular physiology, especially with regard to the mitochondrial compartment. FSK cells were exposed to increasing concentrations of FA, and different cellular parameters were studied. Elevation in intracellular FA level was achieved and was found to be cytotoxic by virtue of both apoptosis and necrosis and was accompanied by both G2/M arrest and reduction in the time spent in S phase. A gene expression assessment by microarray analysis revealed FA affected FSK cells by altering expression of many genes including genes involved in mitochondrial function and electron transport. We were surprised to observe increased DNA double-strand breaks (DSBs) in mitochondria after exposure to FA, as revealed by accumulation of γH2A.X and 53BP1 at mitochondrial DNA foci. This was associated with mitochondrial structural rearrangements, loss of mitochondrial membrane potential and activation of mitophagy. Collectively, these results indicate that an increase in the cellular level of FA can trigger mitochondrial DNA double-strand breaks and dysfunction.

Indexed as

ApoptosisCell CycleCell LineDNA Breaks, Double-StrandedDNA DamageDNA, MitochondrialDNA RepairFibroblastsFormaldehydeHumansMembrane Potential, MitochondrialMitochondriaReactive Oxygen SpeciesDNA, MitochondrialFormaldehydeReactive Oxygen Species

Identifiers

PMID32221313
PMCPMC7101401
OpenAlexW3013904902

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.