Evidence map›Paper›PMID 26980303›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2016

Sulfur Dioxide Contributes to the Cardiac and Mitochondrial Dysfunction in Rats.

Guohua Qin, Meiqiong Wu, Jiaoxia Wang, Zhifang Xu, Jin Xia, Nan Sang

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In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Sodium dithionate (NaToxicology reports · 2022
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  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Sulfur dioxide induces apoptosis via reactive oxygen species generation in rat cardiomyocytes.Environmental science and pollution research international · 2019
    Article
  18. Review
  19. Monitoring SOInternational journal for equity in health · 2017
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Guohua QinThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China.
Meiqiong WuThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China.
Jiaoxia WangThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China.
Zhifang XuThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China.
Jin XiaThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China.
Nan SangThe College of Environmental Science and Resources, Shanxi University, Taiyuan, Shanxi, 030006, China sangnan@sxu.edu.cn.
Shanxi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological studies have demonstrated an association between sulfur dioxide (SO2) and an increase of morbidity and mortality of cardiovascular diseases, such as ischemic heart disease, heart failure, and arrhythmia. Mitochondrion is the most sensitive organelle in myocardium of animals exposed to SO2 Here we study the molecular characterization of mitochondrial dysfunction in cardiac muscles of rat after SO2 exposure. We found that the cytochrome c oxidase (COX) activity, mitochondrial membrane potential (ΔΨm), ATP contents, mitochondrial DNA (mtDNA) contents, and mRNA expression of complexes IV and V subunits encoded by mtDNA were decreased after NaHSO3 treatment in vitro or SO2 inhalation in vivo The mitochondrial dysfunctions were accompanied by depressions of co-activator of peroxisome proliferator activated receptor gamma (PGC-1α), nuclear respiratory factor 1, and mitochondrial transcription factor A (TFAM) mRNA and protein. We observed swollen mitochondria and lower amounts of cristae in hearts of rats after 3.5 mg/m(3) SO2 inhalation for 30 days. Interestingly, NaHSO3 induced mitochondrial dysfunctions marked by ΔΨm and ATP reduction could be inhibited by an antioxidant N-acetyl-L-cysteine (NALC), accompanied by the restoration of transcriptional factors expressions. The cardiac mitochondrial dysfunctions could also be alleviated by overexpression of TFAM. SO2 induced abnormal left ventricular function was restored by NALC in vivo Our findings demonstrate that SO2 induces cardiac and mitochondrial dysfunction. And inhibition of reactive oxygen species and enhancing the transcriptional network controlling mitochondrial biogenesis can mitigate the SO2-induced mitochondrial dysfunction.

Indexed as

AnimalsAntioxidantsCardiotoxicityCell LineDNA, MitochondrialDose-Response Relationship, DrugElectron Transport Complex IVEnergy MetabolismInhalation ExposureMaleMitochondria, HeartMitochondrial Proton-Translocating ATPasesMyocytes, CardiacOxidative StressRats, WistarReactive Oxygen SpeciesAntioxidantscomplex V (mitochondrial oxidative phosphorylation system)DNA, MitochondrialElectron Transport Complex IVMitochondrial Proton-Translocating ATPasesReactive Oxygen Speciessodium hydrogen sulfiteSulfitesSulfur DioxideTfam protein, ratTranscription Factorscardiac muscles.mitochondriareactive oxygen speciessulfur dioxideTFAM

Identifiers

PMID26980303
OpenAlexW2298284872

What OpenQuestion holds

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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.