Evidence map›Paper›PMID 36112262›Full record

ReviewCell biology and toxicology2023

Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.

Ricardo Alva, Maha Mirza, Adam Baiton, Lucas Lazuran, Lyuda Samokysh, Ava Bobinski, Cale Cowan, Alvin Jaimon, Dede Obioru, Tala Al Makhoul and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
16.1field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
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  16. Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025
    Article
  17. Article
  18. Oxygen therapy in the intensive care unit.Medical gas research · 2025
    Review
  19. Review
  20. Article

9 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Ricardo AlvaDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Maha MirzaDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Adam BaitonDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Lucas LazuranDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Lyuda SamokyshDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Ava BobinskiDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Cale CowanDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Alvin JaimonDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Dede ObioruDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Tala Al MakhoulDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Jeffrey A StuartDepartment of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada. jstuart@brocku.ca.
Brock University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In clinical settings, oxygen therapy is administered to preterm neonates and to adults with acute and chronic conditions such as COVID-19, pulmonary fibrosis, sepsis, cardiac arrest, carbon monoxide poisoning, and acute heart failure. In non-clinical settings, divers and astronauts may also receive supplemental oxygen. In addition, under current standard cell culture practices, cells are maintained in atmospheric oxygen, which is several times higher than what most cells experience in vivo. In all the above scenarios, the elevated oxygen levels (hyperoxia) can lead to increased production of reactive oxygen species from mitochondria, NADPH oxidases, and other sources. This can cause cell dysfunction or death. Acute hyperoxia injury impairs various cellular functions, manifesting ultimately as physiological deficits. Chronic hyperoxia, particularly in the neonate, can disrupt development, leading to permanent deficiencies. In this review, we discuss the cellular activities and pathways affected by hyperoxia, as well as strategies that have been developed to ameliorate injury. • Hyperoxia promotes overproduction of reactive oxygen species (ROS). • Hyperoxia dysregulates a variety of signaling pathways, such as the Nrf2, NF-κB and MAPK pathways. • Hyperoxia causes cell death by multiple pathways. • Antioxidants, particularly, mitochondria-targeted antioxidants, have shown promising results as therapeutic agents against oxygen toxicity in animal models.

Indexed as

COVID-19HyperoxiaAnimalsAntioxidantsCell DeathLungOxygenReactive Oxygen SpeciesAntioxidantsOxygenReactive Oxygen SpeciesAntioxidantsCell deathHyperoxiaMitochondriaOxygen toxicityReactive oxygen species

Identifiers

PMID36112262
PMCPMC9483325
OpenAlexW4296038451

What OpenQuestion holds

Textmetadata
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.