Evidence map›Paper›PMID 28454103›Full record

ArticleOncotarget2017

Subchronic arsenism-induced oxidative stress and inflammation contribute to apoptosis through mitochondrial and death receptor dependent pathways in chicken immune organs.

Hongjing Zhao, Ying He, Siwen Li, Xiao Sun, Yu Wang, Yizhi Shao, Zhijun Hou, Mingwei Xing

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

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  8. Fucosylated oligosaccharide Lacto-Food chemistry: X · 2022
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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

8 authors.

Hongjing ZhaoDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Ying HeDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Siwen LiDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Xiao SunDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Yu WangDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Yizhi ShaoDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Zhijun HouDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Mingwei XingDepartment of Physiology, College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In many organ dysfunctions, arsenic and its compounds are well known to induce apoptosis by the mitochondria and death receptor apoptotic pathways in liver and airway. However, it is less reported that which signaling pathways contribute to excessive apoptosis of chicken immune organs, a major target of toxic metals biotransformation, which suffer from subchronic arsenism. In this study, we investigated whether the mitochondria or death receptor apoptotic pathways activated in the immune organs (spleen, thymus and bursa of Fabricius) of one-day-old male Hy-line chickens exposed to arsenic trioxide (As2O3), which were fed on diets supplemented with 0, 0.625, 1.25 and 2.5 mg/kg BW of As2O3 for 30, 60 and 90 days. We found that (1) Oxidative damage and inflammatory response were confirmed in the immune organs of chickens fed on As2O3 diet. (2) Subchronic arsenism induced typical apoptotic changes in ultrastructure. (3) TdT-mediated dUTP Nick-End Labeling (TUNEL) showed that the number of apoptotic cells significantly increased under subchronic arsenism. (4) As2O3-induced apoptosis of immune organs involved in mitochondrial pathway (decrease of B-cell lymphoma-2 (Bcl-2) and increase of protein 53 (p53), Bcl-2 Associated X Protein (Bax), caspase-9, caspase-3) and death receptor pathway (increase of factor associated suicide (Fas) and caspase-8). In conclusion, this work is the first to demonstrate that the activation of mitochondria and death receptor apoptosis pathways can lead to excessive apoptosis in immune organs of chickens, which suffer from subchronic arsenism, meanwhile, oxidative stress as well as subsequent inflammatory is a crucial driver of apoptosis.

Indexed as

AnimalsApoptosisArsenicalsArsenic PoisoningArsenic Trioxidebcl-2-Associated X ProteinBursa of FabriciusCaspase 3Caspase 8Caspase 9ChickensInflammationIn Situ Nick-End LabelingMaleMitochondriaOxidative StressArsenicalsArsenic Trioxidebcl-2-Associated X ProteinCaspase 3Caspase 8Caspase 9OxidesProto-Oncogene Proteins c-bcl-2Receptors, Death Domainapoptosisarsenicchickeninflammationoxidative stress

Identifiers

PMID28454103
PMCPMC5522337

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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.