Cytotoxicity of allyl isothiocyanate on insulin-producing INS-1E cells

cris.virtual.author-orcid0000-0002-5155-0358
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cris.virtualsource.author-orcid9f4dc2c4-beca-4f8b-aafd-53f1e5c550d6
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dc.abstract.enAllyl isothiocyanate (AITC) is the pungent ingredient of brassica species, used as a food additive and flavoring agent, including condiments such as wasabi, horseradish, and mustard. Currently, there is much evidence that AITC modulates glucose and lipids metabolism. Interestingly, AITC has been shown to improve glycaemia, and insulin action along with the induction of a deepened decline in blood insulin levels in T2DM rats. Therefore, in the present study, we characterized the role of AITC at a wide concentration range (5, 10, 25, 50, 100 µM) in controlling viability, proliferation, apoptosis, mitochondrial condition, mRNA expression of encoding pancreatic and duodenal homeobox 1 (Pdx1), and Ins1, Ins2 genes, and insulin content in INS-1E cells. The INS-1E cell line is a suitable, and wellcharacterized model to study beta cell functions. We demonstrate that AITC reduced the viability (p£0.001) (also in the presence of transient receptor potential cation subfamily A member 1 (TRPA1) selective antagonist; HC-030031; p£0.05), and proliferation of INS-1E cells (p£0.001). AITC evoked a significant reduction of mitochondrial membrane potential (p£0.01) and decreased the intracellular level of adenosine triphosphate (ATP) (p£0.001) without influence on reactive oxygen species (ROS) level. Additionally, AITC inhibited the insulin mRNA expression (p£0.001) in INS-1E cells along with insulin content (p£0.05). Mitochondrial dysfunction is proposed to be a significant disruption mechanism of AITC in INS-1E cells, and it was independent of ROS, and the influx of external calcium.
dc.affiliationWydział Medycyny Weterynaryjnej i Nauk o Zwierzętach
dc.affiliation.instituteKatedra Fizjologii, Biochemii i Biostruktury ZwierzÄ…t
dc.contributor.authorOkulicz, Monika
dc.contributor.authorBillert, M.
dc.contributor.authorWojciechowicz, T.
dc.contributor.authorSkrzypski, M.
dc.date.access2024-07-29
dc.date.accessioned2024-08-21T05:36:57Z
dc.date.available2024-08-21T05:36:57Z
dc.date.copyright2024-06-30
dc.date.issued2024-06-30
dc.description.accesstimeat_publication
dc.description.bibliographyil., bibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.if2,0
dc.description.number3
dc.description.points100
dc.description.reviewreview
dc.description.versionfinal_published
dc.description.volume75
dc.identifier.doi10.26402/jpp.2024.3.04
dc.identifier.eissn1899-1505
dc.identifier.issn0867-5910
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/1670
dc.identifier.weblinkhttps://www.jpp.krakow.pl/journal/archive/06_24/articles/04_article.html
dc.languageen
dc.relation.ispartofJournal of Physiology and Pharmacology
dc.relation.pages267-275
dc.rightsOther
dc.sciencecloudsend
dc.share.typeOPEN_JOURNAL
dc.subject.enallyl isothiocyanate
dc.subject.enbeta cells
dc.subject.encell viability
dc.subject.eninsulin expression
dc.subject.encell proliferation
dc.subject.enmitochondrial membrane potential
dc.subject.enadenosine triphosphate
dc.subject.entransient receptor potential cation subfamily A member 1
dc.subject.enpancreatic and duodenal homeobox 1
dc.titleCytotoxicity of allyl isothiocyanate on insulin-producing INS-1E cells
dc.typeJournalArticle
dspace.entity.typePublication
project.funder.nameb.d.