Evidence map›Paper›PMID 33806369›Full record

ArticleInternational journal of molecular sciences2021

A Commonly Used Biocide 2-N-octyl-4-isothiazolin-3-oneInduces Blood-Brain Barrier Dysfunction via Cellular Thiol Modification and Mitochondrial Damage.

Donghyun Kim, Eun-Hye Kim, Sungbin Choi, Kyung-Min Lim, Lu Tie, Arshad Majid, Ok-Nam Bae

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 19 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

7 authors at 4 institutions in 3 countries.

Donghyun KimCollege of Pharmacy Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea.
Eun-Hye KimCollege of Pharmacy Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea.
Sungbin ChoiCollege of Pharmacy Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea.
Kyung-Min LimCollege of Pharmacy, Ewha Womans University, Seoul 03760, Korea.ORCID 0000-0002-1517-7680
Lu TieDepartment of Pharmacology, School of Basic Medical Science, Peking University, Beijing 100083, China.ORCID 0000-0003-4755-2091
Arshad MajidSheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield S10 2TN, UK.
Ok-Nam BaeCollege of Pharmacy Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea.ORCID 0000-0003-0583-2116
Hanyang University · KREwha Womans University · KRPeking University · CNUniversity of Sheffield · GB

Funding

Korea Environmental Industry and Technology Institute 2019002490005 1485016231, 2019002490004 1485016253, 2020002970001Medical Research Council MR/R005923/1
6 · The paper itself

Abstract

Isothiazolinone (IT) biocides are potent antibacterial substances commonly used as preservatives or disinfectants, and 2-n-Octyl-4-isothiazolin-3-one (OIT; octhilinone) is a common IT biocide that is present in leather products, glue, paints, and cleaning products. Although humans are exposed to OIT through personal and industrial use, the potentially deleterious effects of OIT on human health are still unknown. To investigate the effects of OIT on the vascular system, which is continuously exposed to xenobiotics through systemic circulation, we treated brain endothelial cells with OIT. OIT treatment significantly activated caspase-3-mediated apoptosis and reduced the bioenergetic function of mitochondria in a bEnd.3 cell-based in vitro blood-brain barrier (BBB) model. Interestingly, OIT significantly altered the thiol redox status, as evidenced by reduced glutathione levels and protein S-nitrosylation. The endothelial barrier function of bEnd.3 cells was significantly impaired by OIT treatment. OIT affected mitochondrial dynamics through mitophagy and altered mitochondrial morphology in bEnd.3 cells. N-acetyl cysteine significantly reversed the effects of OIT on the metabolic capacity and endothelial function of bEnd.3 cells. Taken together, we demonstrated that the alteration of the thiol redox status and mitochondrial damage contributed to OIT-induced BBB dysfunction, and we hope that our findings will improve our understanding of the potential hazardous health effects of IT biocides.

Indexed as

AcetylcysteineAnimalsAntioxidantsBlood-Brain BarrierBrainCell DeathCell LineDisinfectantsEndothelial CellsEnergy MetabolismHumansMembrane Potential, MitochondrialMiceMitochondriaProteolysisReactive Oxygen Species2-n-octyl-4-isothiazolin-3-oneAcetylcysteineAntioxidantsDisinfectantsReactive Oxygen SpeciesSulfhydryl CompoundsThiazolesTight Junction Proteins2-n-Octyl-4-isothiazolin-3-one (OIT)blood–brain barrier (BBB) modelisothiazolinone (IT) biocidemitochondrial dysfunctionoxidative stressprotein S-nitrosylation (SNO)

Identifiers

PMID33806369
PMCPMC7975974
OpenAlexW3133644561

What OpenQuestion holds

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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.