Evidence map›Paper›PMID 24250680›Full record

ArticleIranian journal of pharmaceutical research : IJPR2013

Toxicity of Arsenic (III) on Isolated Liver Mitochondria: A New Mechanistic Approach.

Mir-Jamal Hosseini, Fatemeh Shaki, Mahmoud Ghazi-Khansari, Jalal Pourahmad

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of pharmaceutical research : IJPR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Continuing the Conversation About Arsenic.Integrative medicine (Encinitas, Calif.) · 2024
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
  13. Strategies for Protecting Mitochondria From Metals and Chemicals.Integrative medicine (Encinitas, Calif.) · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. An Overview: The Toxicity ofInternational journal of molecular sciences · 2021
    Review
  19. Review
  20. 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

4 authors at 2 institutions in 1 country.

Mir-Jamal HosseiniFaculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ; Department of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran. ; Student Research Committee, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fatemeh Shaki
Mahmoud Ghazi-Khansari
Jalal Pourahmad
Shahid Beheshti University of Medical Sciences · IRZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic exposure mainly through food and water has been shown to be associated with increased incidence of numerous cancers and non-cancer harmful health. It is also used in cancer chemotherapy and treatment of several cancer types due to its apoptogenic effects in the various cancer and normal cell lines. We have already reported that liver is the storage site and important target organ in As (III) toxicity and recently, it has been suggested that hepatic toxicity of arsenic could be resulted from impairment of the liver mitochondria. In this study, interaction of As (III) with freshly isolated rat mitochondria was investigated. We determined different mitochondrial toxicity factors as well as mitochondrial sources of ROS formation using specific substrates and inhibitors following addition of As (III) to the mitochondria. Our results showed that arsenic (III) increased mitochondrial ROS formation, lipid peroxidation and mitochondrial membrane potential collapse, cytochrome c release and mitochondrial swelling in a concentration dependent manner. Addition of As (III) in to the isolated mitochondria, inhibited complexes I and II leading to disruption of mitochondrial electron transfer chain, decreased mitochondrial ATP content and ROS formation.

Indexed as

Arsenic (III)Complex IComplex IImitochondriaReactive Oxygen Species

Identifiers

PMID24250680
PMCPMC3813354
OpenAlexW2096425711

What OpenQuestion holds

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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.