Evidence map›Paper›PMID 26294939›Full record

ArticleOxidative medicine and cellular longevity2015

Mitochondrial Respiratory Chain Inhibitors Involved in ROS Production Induced by Acute High Concentrations of Iodide and the Effects of SOD as a Protective Factor.

Lingyan Wang, Qi Duan, Tingting Wang, Mohamed Ahmed, Na Zhang, Yongmei Li, Lanying Li, Xiaomei Yao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

39 citing papers in PubMed, 60 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

8 authors at 1 institution in 1 country.

Lingyan WangDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Qi DuanDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Tingting WangDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Mohamed AhmedDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Na ZhangDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Yongmei LiKey Lab of Hormones and Development Ministry of Health, Institute of Endocrinology, Metabolic Disease Hospital, Tianjin Medical University, Tianjin 300070, China.
Lanying LiKey Lab of Hormones and Development Ministry of Health, Institute of Endocrinology, Metabolic Disease Hospital, Tianjin Medical University, Tianjin 300070, China.
Xiaomei YaoDepartment of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major source of reactive oxygen species (ROS) generation is the mitochondria. By using flow cytometry of the mitochondrial fluorescent probe, MitoSOX Red, western blot of mitochondrial ROS scavenger Peroxiredoxin (Prx) 3 and fluorescence immunostaining, ELISA of cleaved caspases 3 and 9, and TUNEL staining, we demonstrated that exposure to 100 μM KI for 2 hours significantly increased mitochondrial superoxide production and Prx 3 protein expression with increased expressions of cleaved caspases 3 and 9. Besides, we indicated that superoxide dismutase (SOD) at 1000 unit/mL attenuated the increase in mitochondrial superoxide production, Prx 3 protein expression, and lactate dehydrogenase (LDH) release and improved the relative cell viability at 100 μM KI exposure. However, SOD inhibitor diethyldithiocarbamic acid (DETC) (2 mM), Rotenone (0.5 μM), a mitochondrial complex I inhibitor, and Antimycin A (10 μM), a complex III inhibitor, caused an increase in mitochondrial superoxide production, Prx 3 protein expression, and LDH release and decreased the relative cell viability. We conclude that the inhibitors of mitochondrial respiratory chain complex I or III may be involved in oxidative stress caused by elevated concentrations of iodide, and SOD demonstrates its protective effect on the Fischer rat thyroid cell line (FRTL) cells.

Indexed as

Electron Transport Complex IIodidesMitochondrial MembranesReactive Oxygen SpeciesSuperoxide DismutaseElectron Transport Complex IIodidesReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID26294939
PMCPMC4532905
OpenAlexW1541795301

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.