Evidence map›Paper›PMID 29062904›Full record

ArticleClinical and experimental hepatology2017

Ammonia-induced mitochondrial dysfunction and energy metabolism disturbances in isolated brain and liver mitochondria, and the effect of taurine administration: relevance to hepatic encephalopathy treatment.

Hossein Niknahad, Akram Jamshidzadeh, Reza Heidari, Mahdi Zarei, Mohammad Mehdi Ommati

Open access · diamondAbstract read
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Article in Clinical and experimental hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 99 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

5 authors at 2 institutions in 1 country.

Hossein NiknahadPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Akram JamshidzadehPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Reza HeidariPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Mahdi ZareiPharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Mohammad Mehdi OmmatiDepartment of Animal Sciences, School of Agriculture, Shiraz University, Shiraz, Iran.
Shiraz University of Medical Sciences · IRShiraz University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAmmonia-induced oxidative stress, mitochondrial dysfunction, and energy crisis are known as some the major mechanisms of brain injury in hepatic encephalopathy (HE). Hyperammonemia also affects the liver and hepatocytes. Therefore, targeting mitochondria seems to be a therapeutic point of intervention in the treatment of HE. Taurine is an abundant amino acid in the human body. Several biological functions including the mitochondrial protective properties are attributed to this amino acid. The aim of this study is to evaluate the effect of taurine administration on ammonia-induced mitochondrial dysfunction. MATERIAL AND

methodsIsolated mice liver and brain mitochondria were exposed to different concentrations of ammonia (1, 5, 10, and 20 mM) and taurine (1, 5, and 10 mM), and several mitochondrial indices were assessed.

resultsIt was found that ammonia inhibited mitochondrial dehydrogenases activity caused collapse of mitochondrial membrane potential (MMP), induced mitochondrial swelling (MPP), and increased reactive oxygen species (ROS) in isolated liver and brain mitochondria. Furthermore, a significant amount of lipid peroxidation (LPO), along with glutathione (GSH) and ATP depletion, was detected in ammonia exposed mitochondria. Taurine administration (5 and 10 mM) mitigated ammonia-induced mitochondrial dysfunction.

conclusionsThe current investigation demonstrates that taurine is instrumental in preserving brain and liver mitochondrial function in a hyperammonemic environment. The data suggest taurine as a potential protective agent with a therapeutic capability against hepatic encephalopathy and hyperammonemia.

Indexed as

amino acidbioenergeticsbrain injuryhepatic encephalopathytaurine

Identifiers

PMID29062904
PMCPMC5649485
OpenAlexW2753006837

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LicenceCC BY-NC-SA
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Registered trials

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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.