Evidence map›Paper›PMID 33866498›Full record

ArticleBiological trace element research2022

Protective Effects of Alpha Lipoic Acid Against Arsenic Induced Oxidative Stress in Isolated Rat Liver Mitochondria.

Farzan Mozaffarian, Mohammad Amin Dehghani, Atefeh Raesi Vanani, Masoud Mahdavinia

Abstract read
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In one paragraph

Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Lipoic Acid Attenuates Lipopolysaccharide- andInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Alpha-lipoic acid, as an effective agent against toxic elements: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
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 1 institution in 1 country.

Farzan MozaffarianToxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad Amin DehghaniToxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Atefeh Raesi VananiToxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Masoud MahdaviniaToxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. mahdavimasoud@yahoo.com.ORCID http://orcid.org/0000-0001-9448-1500
Ahvaz Jundishapur University of Medical Sciences · IR

Funding

Ahvaz Jundishapur University of Medical Sciences B-98038
6 · The paper itself

Abstract

Arsenic as a heavy metal and toxic pollutant has been established that has the hepatotoxic effect in animal and human models. Previous studies showed that mitochondria as the first target of arsenic toxicity has a pathogenic role in liver diseases. This study investigated alpha lipoic acid (ALA) as an antioxidant could ameliorate against liver toxicity induced by arsenic in rat mitochondria. First, mitochondria were isolated by the liver tissue centrifugation protocol. Then, isolated mitochondria were exposed with different concentrations of ALA and arsenic in different times for receiving the optimum dose and time. Finally, mitochondria were pretreated with the optimum concentrations and times of ALA and then treated with optimum concentration and time of arsenic (160 μg/ml; 30 min). The results demonstrated a significant decrease in total mitochondrial dehydrogenase activity (mitochondrial complex II) by 3, 4 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay after arsenic exposure. Mitochondria treated with arsenic also showed a significant increase in ROS generation, MMP, and MDA levels. The activity of mitochondrial catalase and mitochondrial GSH significantly decreased after exposure of mitochondria with arsenic. Pretreatment of mitochondria with ALA improved mitochondrial complex II activity; decreased mitochondrial membrane damage, MDA, and ROS amounts; and ameliorated mitochondrial GSH levels and mitochondrial catalase activity. These findings revealed that arsenic induced oxidative stress and mitochondria dysfunction, while ALA improved mitochondrial function through increasing of antioxidant defense or preserving of complex II, but suggested that ALA could prevent from mitochondria dysfunction.

Indexed as

ArsenicThioctic AcidAnimalsMitochondriaMitochondria, LiverOxidative StressRatsReactive Oxygen SpeciesArsenicReactive Oxygen SpeciesThioctic AcidAlpha lipoic acidArsenicMitochondrialOxidative stressRat

Identifiers

PMID33866498
OpenAlexW3153373132

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.