Evidence map›Paper›PMID 37915488›Full record

ArticleToxicology research2023

Metabolic disturbance and transcriptomic changes induced by methyl triclosan in human hepatocyte L02 cells.

Jing An, Yuting Yi, Jingjing Jiang, Weiwei Yao, Guofa Ren, Yu Shang

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026
    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

6 authors at 1 institution in 1 country.

Jing AnInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.ORCID https://orcid.org/0000-0003-0885-8979
Yuting YiInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.
Jingjing JiangInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.ORCID https://orcid.org/0000-0002-2008-5326
Weiwei YaoInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.
Guofa RenInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.
Yu ShangInstitute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.
Shanghai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMethyl triclosan (MTCS) is one of the biomethylated by-products of triclosan (TCS). With the increasing use of TCS, the adverse effects of MTCS have attracted extensive attention in recent years. The purpose of this study was to investigate the cytotoxicity of MTCS and to explore the underlining mechanism using human hepatocyte L02 cells as in vitro model.

resultsThe cytotoxicity results revealed that MTCS could inhibit cell viability, disturb the ratio of reduced glutathione (GSH) and oxidized glutathione (GSSG), and reduce the mitochondrial membrane potential (MMP) in a dose-dependent manner. In addition, MTCS exposure significantly promoted the cellular metabolic process, including enhanced conversion of glucose to lactic acid, and elevated content of intracellular triglyceride (TG) and total cholesterol (TC). RNA-sequencing and bioinformatics analysis indicated disorder of glucose and lipid metabolism was significantly induced after MTCS exposure. Protein-protein interaction network analysis and node identification suggested that Serine hydroxy methyltransferase 2 (SHMT2), Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2), Asparagine synthetase (ASNS) and Phosphoglycerate dehydrogenase (PHGDH) are potential molecular markers of metabolism imbalance induced by MTCS.

conclusionThese results demonstrated that oxidative stress and metabolism dysregulation might be involved in the cytotoxicity of MTCS in L02 cells.

Indexed as

metabolism dysregulationmethyl triclosanoxidative stressRNA-sequencing

Identifiers

PMID37915488
PMCPMC10615820
OpenAlexW4386726999

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.