Academic Thesis

Basic information

Name Higashi Tunehito
Belonging department
Occupation name
researchmap researcher code 5000085325
researchmap agency Okayama University of Science

Title

Intracellular Ca2+ is an essential factor for cell damage induced by unsaturated carbonyl compounds

Bibliography Type

 

Author

Tsunehito Higashi
Yosuke Mai
Yuichi Mazaki
Soichi Miwa

Summary

The unsaturated carbonyl compounds are known as the environmental pollutants. Acrolein (ACR) and methyl vinyl ketone (MVK) are representative unsaturated carbonyl compounds. ACR is contained in smoke, automobile exhaust, industrial waste, and several foods. MVK is widely used as the industrial chemical. Although ACR and MVK are highly toxic, the molecular mechanism for their cytotoxicity has been unclear. We have previously reported that ACR and MVK are major cytotoxic compounds in the gas phase of cigarette smoke, and protein kinase C (PKC) inhibitor and NADPH oxidases inhibitor partially rescued cells from ACR-or MVK-induced cell death (Noya et al., Toxicology, 314, 1-10, 2013). PKC translocation, which is hallmark for PKC activation, and cell damage were induced by treatment of cultured cells with ACR or MVK. Intracellular Ca2+ chelator completely suppressed ACR-or MVK-induced PKC translocation to the cell membrane and cell damage, while extracellular Ca2+ chelator had no effects on ACR- and MVK-induced cytotoxicity. These results suggest that intracellular Ca2+ is an essential factor for cell damage caused by both PKC-dependent and PKC-independent pathways, and mobilization of Ca2+ from intracellular Ca2+ stores is induced by ACR or MVK. (C) 2017, The Society for Biotechnology, Japan. All rights reserved.

Magazine(name)

JOURNAL OF BIOSCIENCE AND BIOENGINEERING

Publisher

SOC BIOSCIENCE BIOENGINEERING JAPAN

Volume

124

Number Of Pages

6

StartingPage

680

EndingPage

684

Date of Issue

2017-12

Referee

Exist

Invited

Not exist

Language

English

Thesis Type

Research papers (academic journals)

ISSN

 

DOI

10.1016/j.jbiosc.2017.07.003

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PMID

 

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DBLP ID