Cytotoxicity of allyl isothiocyanate on insulin-producing INS-1E cells
Type
Journal article
Language
English
Date issued
June 30, 2024
Author
Faculty
Wydział Medycyny Weterynaryjnej i Nauk o Zwierzętach
Journal
Journal of Physiology and Pharmacology
ISSN
0867-5910
Volume
75
Number
3
Pages from-to
267-275
Abstract (EN)
Allyl 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.
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.
License
Other
Open access date
June 30, 2024