Evidence map›Paper›PMID 36394988›Full record

ArticleEnvironmental science & technology2022

Superoxide Release by Macrophages through NADPH Oxidase Activation Dominating Chemistry by Isoprene Secondary Organic Aerosols and Quinones to Cause Oxidative Damage on Membranes.

Ting Fang, Yu-Kai Huang, Jinlai Wei, Jessica E Monterrosa Mena, Pascale S J Lakey, Michael T Kleinman, Michelle A Digman, Manabu Shiraiwa

Open access · hybridAbstract read
In one paragraph

Article in Environmental science & technology, 2022. 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
2.7field-weighted citation impact, top 10% 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, 27 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 1 institution in 1 country.

Ting FangDepartment of Chemistry, University of California, Irvine 92697, California, United States.ORCID 0000-0002-4845-2749
Yu-Kai HuangDepartment of Biomedical Engineering, University of California, Irvine 92697, California, United States.
Jinlai WeiDepartment of Chemistry, University of California, Irvine 92697, California, United States.ORCID 0000-0002-4741-9015
Jessica E Monterrosa MenaDivision of Occupational and Environmental Medicine, University of California, Irvine 92697, California, United States.ORCID 0000-0002-3315-4431
Pascale S J LakeyDepartment of Chemistry, University of California, Irvine 92697, California, United States.ORCID 0000-0003-2923-4073
Michael T KleinmanDivision of Occupational and Environmental Medicine, University of California, Irvine 92697, California, United States.
Michelle A DigmanDepartment of Biomedical Engineering, University of California, Irvine 92697, California, United States.
Manabu ShiraiwaDepartment of Chemistry, University of California, Irvine 92697, California, United States.ORCID 0000-0003-2532-5373
University of California, Irvine · US

Funding

TRD4: Phasor analysisP41GM103540 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRATTON, ENRICO · 2012 to 2020
$12.5M
NIGMS NIH HHS P41 GM103540
6 · The paper itself

Abstract

Oxidative stress mediated by reactive oxygen species (ROS) is a key process for adverse aerosol health effects. Secondary organic aerosols (SOA) account for a major fraction of fine particulate matter, and their inhalation and deposition into the respiratory tract causes the formation of ROS by chemical and cellular processes, but their relative contributions are hardly quantified and their link to oxidative stress remains uncertain. Here, we quantified cellular and chemical superoxide generation by 9,10-phenanthrenequinone (PQN) and isoprene SOA using a chemiluminescence assay combined with electron paramagnetic resonance spectroscopy as well as kinetic modeling. We also applied cellular imaging techniques to study the cellular mechanism of superoxide release and oxidative damage on cell membranes. We show that PQN and isoprene SOA activate NADPH oxidase in macrophages to release massive amounts of superoxide, overwhelming the superoxide formation by aqueous chemical reactions in the epithelial lining fluid. The activation dose for PQN is 2 orders of magnitude lower than that of isoprene SOA, suggesting that quinones are more toxic. While higher exposures trigger cellular antioxidant response elements, the released ROS induce oxidative damage to the cell membrane through lipid peroxidation. Such mechanistic and quantitative understandings provide a basis for further elucidation of adverse health effects and oxidative stress by fine particulate matter.

Indexed as

Air PollutantsSuperoxidesAerosolsButadienesHemiterpenesMacrophagesNADPH OxidasesOxidative StressParticulate MatterQuinonesReactive Oxygen SpeciesAerosolsAir PollutantsButadienesHemiterpenesisopreneNADPH OxidasesParticulate MatterQuinonesReactive Oxygen SpeciesSuperoxidesantioxidant response elementsaqueous chemistrycell membrane fluiditycellular mechanismepithelial lining fluidlipid peroxidationreactive oxygen species

Identifiers

PMID36394988
PMCPMC9730850
OpenAlexW4309202294

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.