Evidence map›Paper›PMID 27667976›Full record

ArticleFrontiers in physiology2016

Microcystin-LR Induced Apoptosis in Rat Sertoli Cells via the Mitochondrial Caspase-Dependent Pathway: Role of Reactive Oxygen Species.

Hui Huang, Chuanrui Liu, Xiaoli Fu, Shenshen Zhang, Yongjuan Xin, Yang Li, Lijian Xue, Xuemin Cheng, Huizhen Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 42 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

9 authors at 1 institution in 1 country.

Hui HuangDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Chuanrui LiuDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Xiaoli FuDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Shenshen ZhangDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Yongjuan XinDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Yang LiDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Lijian XueDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Xuemin ChengDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Huizhen ZhangDepartment of Environmental Health, School of Public Health, Zhengzhou University Zhengzhou, China.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microcystins (MCs), the secondary metabolites of blue-green algae, are ubiquitous and major cyanotoxin contaminants. Besides the hepatopancreas/liver, the reproductive system is regarded as the most important target organ for MCs. Although reactive oxygen species (ROS) have been implicated in MCs-induced reproductive toxicity, the role of MCs in this pathway remains unclear. In the present study, Sertoli cells were employed to investigate apoptotic death involved in male reproductive toxicity of microcystin-LR (MC-LR). After exposure to various concentrations of MC-LR for 24 h, the growth of Sertoli cells was concentration-dependently decreased with an IC50 of ~32 μg/mL. Mitochondria-mediated apoptotic changes were observed in Sertoli cells exposed to 8, 16, and 32 μg/mL MC-LR including the increased expression of caspase pathway proteins, collapse of mitochondrial membrane potential (MMP), and generation of ROS. Pretreatment with a global caspase inhibitor was found to depress the activation of caspases, and eventually increased the survival rate of Sertoli cells, implying that the mitochondrial caspases pathway is involved in MC-LR-induced apoptosis. Furthermore, N-acetyl-l-cysteine attenuated the MC-LR-induced intracellular ROS generation, MMP collapse and cytochrome c release, resulting in the inhibition of apoptosis. Taken together, the observed results suggested that MC-LR induced apoptotic death of Sertoli cells by the activation of mitochondrial caspases cascade, while its effects on the ROS-mediated signaling pathway may contribute toward the initiation of mitochondrial dysfunction.

Indexed as

apoptosismicrocystin-LR (MC-LR)mitochondriareactive oxygen species (ROS)Sertoli cells

Identifiers

PMID27667976
PMCPMC5016609
OpenAlexW2515470583

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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.