Evidence map›Paper›PMID 31884112›Full record

ArticleToxicology letters2020

Toxic consequences and oxidative protein carbonylation from chloropicrin exposure in human corneal epithelial cells.

Dinesh G Goswami, Rama Kant, David A Ammar, Chapla Agarwal, Joe Gomez, Rajesh Agarwal, Laura M Saba, Kristofer S Fritz, Neera Tewari-Singh

Open access · greenAbstract read
In one paragraph

Article in Toxicology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  12. Ocular Surface - Merging Challenges and Opportunities.Translational vision science & technology · 2020
    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

9 authors at 1 institution in 1 country.

Dinesh G GoswamiDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Rama KantDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
David A AmmarDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Chapla AgarwalDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Joe GomezDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Rajesh AgarwalDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Laura M SabaDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Kristofer S FritzDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA.
Neera Tewari-SinghDepartment of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado, 80045, USA; Department of Pharmacology & Toxicology, Michigan State University, East Lansing, Michigan, 48824, USA. Electronic address: tewarisi@msu.edu.
University of Colorado Anschutz Medical Campus · US

Funding

Effective Therapies for Ocular Injuries by Vesicating AgentsU01EY023143 · NEI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2012 to 2016
$3.9M
NEI NIH HHS U01 EY023143
6 · The paper itself

Abstract

Chloropicrin (CP), a warfare agent now majorly used as a soil pesticide, is a strong irritating and lacrimating compound with devastating toxic effects. To elucidate the mechanism of its ocular toxicity, toxic effects of CP (0-100 μM) were studied in primary human corneal epithelial (HCE) cells. CP exposure resulted in reduced HCE cell viability and increased apoptotic cell death with an up-regulation of cleaved caspase-3 and poly ADP ribose polymerase indicating their contribution in CP-induced apoptotic cell death. Following CP exposure, cells exhibited increased expression of heme oxygenase-1, and phosphorylation of H2A.X and p53 as well as 4-hydroxynonenal adduct formation, suggesting oxidative stress, DNA damage and lipid peroxidation. CP also caused increases in mitogen activated protein kinase-c-Jun N-terminal kinase and inflammatory mediator cyclooxygenase-2. Proteomic analysis revealed an increase in the carbonylation of 179 proteins and enrichment of pathways (including proteasome pathway and catabolic process) in HCE cells following CP exposure. CP-induced oxidative stress and lipid peroxidation can enhance protein carbonylation, prompting alterations in corneal epithelial proteins as well as perturbing signaling pathways resulting in toxic effects. Pathways and major processes identified following CP exposure could be lead-hit targets for further biochemical and molecular characterization as well as therapeutic intervention.

Indexed as

ApoptosisCaspase 3Cells, CulturedCyclooxygenase 2DNA DamageEpithelial CellsEpithelium, CornealHeme Oxygenase-1HistonesHumansHydrocarbons, ChlorinatedInflammation MediatorsJNK Mitogen-Activated Protein KinasesLipid PeroxidationOxidative StressPesticidesCASP3 protein, humanCaspase 3chloropicrinCyclooxygenase 2H2AX protein, humanHeme Oxygenase-1HistonesHMOX1 protein, humanHydrocarbons, ChlorinatedInflammation MediatorsJNK Mitogen-Activated Protein KinasesPesticidesPoly(ADP-ribose) PolymerasesPTGS2 protein, humanTP53 protein, humanTumor Suppressor Protein p53ChloropicrinCorneal injuryOxidative stressPesticideProtein carbonylation

Identifiers

PMID31884112
PMCPMC11249040
OpenAlexW2997534058

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.