Evidence map›Paper›PMID 19326901›Full record

ArticleChemical research in toxicology2009

Ascorbic acid promotes detoxification and elimination of 4-hydroxy-2(E)-nonenal in human monocytic THP-1 cells.

Cristobal L Miranda, Ralph L Reed, Heather C Kuiper, Susan Alber, Jan F Stevens

Open access · greenAbstract read
In one paragraph

Article in Chemical research in toxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  4. Organoiridium Complexes Enhance Cellular Defense Against Reactive Aldehydes Species.Chemistry (Weinheim an der Bergstrasse, Germany) · 2023
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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 1 institution in 1 country.

Cristobal L MirandaLinus Pauling Institute and the Departments of Pharmaceutical Sciences and Statistics, Oregon State University, Corvallis, Oregon 97331, USA.
Ralph L Reed
Heather C Kuiper
Susan Alber
Jan F Stevens
Oregon State University · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Ascorbylation of Oxidized Lipids and AtherosclerosisR01HL081721 · NHLBI · OREGON STATE UNIVERSITY · PI STEVENS, JAN FREDERIK · 2006 to 2010
$1.5M
HYBRID TRIPLE QUADRUPOLE LINEAR ION TRAP MASS SPECTROMETER: PROSTATE CANCERS10RR022589 · NCRR · OREGON STATE UNIVERSITY · PI STEVENS, JAN FREDERIK · 2006 to 2006
$343k
NCRR NIH HHS S10 RR022589NCRR NIH HHS S10RR022589NHLBI NIH HHS R01 HL081721NHLBI NIH HHS R01HL081721NIEHS NIH HHS P30 ES000210NIEHS NIH HHS P30ES000210
6 · The paper itself

Abstract

4-Hydroxy-2(E)-nonenal (HNE), a reactive aldehyde derived from oxidized lipids, has been implicated in the pathogenesis of cardiovascular and neurological diseases, in part by its ability to induce oxidative stress and by protein carbonylation in target cells. The effects of intracellular ascorbic acid (vitamin C) on HNE-induced cytotoxicity and protein carbonylation were investigated in human THP-1 monocytic leukemia cells. HNE treatment of these cells resulted in apoptosis, necrosis, and protein carbonylation. Ascorbic acid accumulated in the cells at concentrations of 6.4 or 8.9 mM after treatment with 0.1 or 1 mM ascorbate in the medium for 18 h. Pretreatment of cells with 1.0 mM ascorbate decreased HNE-induced formation of reactive oxygen species and formation of protein carbonyls. The protective effects of ascorbate were associated with an increase in the formation of GSH-HNE conjugate and its phase 1 metabolites, measured by LC-MS/MS, and with increased transport of GSH conjugates from the cells into the medium. Ascorbate pretreatment enhanced the efflux of the multidrug resistant protein (MRP) substrate, carboxy-2',7'-dichlorofluorescein (CDF), and it prevented the HNE-induced inhibition of CDF export from THP-1 cells, suggesting that the protective effect of ascorbate against HNE cytotoxicity is through modulation of MRP-mediated transport of GSH-HNE conjugate metabolites. The formation of ascorbate adducts of HNE was observed in the cell exposure experiments, but it represented a minor pathway contributing to the elimination of HNE and to the protective effects of ascorbate.

Indexed as

AldehydesApoptosisAscorbic AcidBiological TransportCaspase 3FluoresceinsGlutathioneHumansInactivation, MetabolicLeukemiaProtein CarbonylationTumor Cells, Cultured4-hydroxy-2-nonenal5(6)-carboxy-2',7'-dichlorofluoresceinAldehydesAscorbic AcidCaspase 3FluoresceinsGlutathione

Identifiers

PMID19326901
PMCPMC2730585
OpenAlexW2037634222

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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.