Evidence map›Paper›PMID 21850523›Full record

ArticleCell biology and toxicology2011

Increased oxidative stress and cytotoxicity by hydrogen sulfide in HepG2 cells overexpressing cytochrome P450 2E1.

Andres A Caro, Sarah Thompson, Jonathan Tackett

Abstract read
In one paragraph

Article in Cell biology and toxicology, 2011. 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
1.0field-weighted citation impact, top 25% 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, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. SQOR as a metabolic rheostat of HFrontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Hydrogen Sulfide and its Interaction with Other Players in Inflammation.Advances in experimental medicine and biology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Hydrogen sulfide and translational medicine.Acta pharmacologica Sinica · 2013
    Review
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

3 authors at 2 institutions in 1 country.

Andres A CaroChemistry Department, Hendrix College, Conway, AR 72032, USA. caro@hendrix.edu
Sarah Thompson
Jonathan Tackett
Conway School of Landscape Design · USHendrix College · US

Funding

VIRULENCE MECHANISMS IN ESCHERICHIA COLIP20RR016460 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI HENSLEY, LORI · 2001 to 2011
$33.1M
NCRR NIH HHS P20 RR016460NCRR NIH HHS P20 RR-16460
6 · The paper itself

Abstract

The main objectives of this work were to evaluate the effects of hydrogen sulfide on oxidative stress and cytotoxicity parameters in HepG2 cells and to assess the extent to which cytochrome P450 2E1 (CYP2E1) activity modulates the effects of hydrogen sulfide on oxidative stress and cytotoxicity. Sodium hydrosulfide (NaHS) caused time- and concentration-dependent cytotoxicity in both non-P450-expressing HepG2 cells (C34 cells) and CYP2E1-overexpressing HepG2 cells (E47 cells); however, NaHS-dependent cytotoxicity was higher in E47 than C34 cells. Cytotoxicity by NaHS in C34 and E47 cells was mainly necrotic in nature and associated with an early decrease in mitochondrial membrane potential. NaHS caused increased oxidation of lipophilic (C11-BODIPY(581/591)) and hydrophilic (DCFH-DA) probes only in E47 cells, at a time point prior to overt cytotoxicity. Trolox, an amphipathic antioxidant, partially inhibited both the cytotoxicity and the increased oxidative stress detected in E47 cells exposed to NaHS. Cell-permeable iron chelators and CYP2E1 inhibitors significantly inhibited the oxidation of C11-BODIPY(581/591) in E47 cells in the presence of NaHS. NaHS produced lipid peroxidation and cytotoxicity in E47 cells supplemented with a representative polyunsaturated fatty acid (docosahexaenoic acid) but not in C34 cells; these effects were inhibited by α-tocopherol, a lipophilic antioxidant. These data suggest that CYP2E1 enhances H(2)S-dependent cytotoxicity in HepG2 cells through the generation of iron-dependent oxidative stress and lipid peroxidation.

Indexed as

Cytochrome P-450 CYP2E1alpha-TocopherolAntioxidantsBlotting, WesternChromansDose-Response Relationship, DrugFluorescent DyesGene ExpressionHepatocytesHep G2 CellsHumansHydrogen SulfideHydrophobic and Hydrophilic InteractionsLipid PeroxidationMembrane Potential, MitochondrialMitochondria6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acidalpha-TocopherolAntioxidantsChromansCytochrome P-450 CYP2E1Fluorescent DyesHydrogen SulfideReactive Oxygen Speciessodium bisulfideSulfides

Identifiers

PMID21850523
PMCPMC3557813
OpenAlexW2073743482

What OpenQuestion holds

Textmetadata
LicenceTDM
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.