Study of the cytotoxic effects of 2,5-diaziridinyl-3,6-dimethyl-1,4-benzoquinone (MeDZQ) in mouse hepatoma cells

Authors

  • Rasa Jarasiene-Burinskaja Department of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, Sauletekio av. 7, LT-10223 Vilnius, Lithuania
  • Milda Alksne Department of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, Sauletekio av. 7, LT-10223 Vilnius, Lithuania
  • Violeta Bartuskiene Department of Anatomy, Histology and Anthropology, Faculty of Medicine, Vilnius University, M. K. Ciurlionio str. 21, LT-03101 Vilnius, Lithuania
  • Violeta Voisniene Department of Chemistry and Bioengineering, Vilnius Gediminas Technical University, Sauletekio av. 11, LT-10223 Vilnius, Lithuania
  • Jaroslav Burinskij Department of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, Sauletekio av. 7, LT-10223 Vilnius, Lithuania
  • Narimantas Cenas Department of Xenobiotics Biochemistry, Institute of Biochemistry, Life Sciences Center, Vilnius University, Sauletekio av. 7, LT-10223 Vilnius, Lithuania
  • Virginija Bukelskiene Department of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, Sauletekio av. 7, LT-10223 Vilnius, Lithuania

DOI:

https://doi.org/10.17179/excli2016-783

Keywords:

aziridinylbenzoquinones, cytotoxicity, cell signaling, cell death, MeDZQ

Abstract

A number of quinones have been shown to be efficient anticancer agents. However, some mechanisms of their action, in particular cell signaling are not well understood. The aim of this study was to partly fill this gap by characterizing the mode of cytotoxicity of 2,5-diaziridinyl-3,6-dimethyl-1,4-benzoquinone (MeDZQ) in malignant mouse hepatoma cells (MH-22A) with regard to the expression and activation of main molecules in MAPK cell signaling pathway. The study revealed unequal roles of MAP kinases in MeDZQ-induced cell death: the compound did not induce significant changes in ERK expression or its phosphorylation; JNK appeared to be responsible for cell survival, however, p38 kinase was shown to be involved in cell death. In order to assess the enzymatic activation mechanisms responsible for the action of MeDZQ, we have also found that the antioxidant N,N'-diphenyl-p-phenylene diamine, the iron-chelating agent desferrioxamine, and DT-diaphorase inhibitor, dicoumarol, partly protected the cells from MeDZQ cytotoxicity. It points to parallel oxidative stress and bioreductive alkylation modes of the cytotoxicity of MeDZQ.

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Published

2017-03-06

How to Cite

Jarasiene-Burinskaja, R., Alksne, M., Bartuskiene, V., Voisniene, V., Burinskij, J., Cenas, N., & Bukelskiene, V. (2017). Study of the cytotoxic effects of 2,5-diaziridinyl-3,6-dimethyl-1,4-benzoquinone (MeDZQ) in mouse hepatoma cells. EXCLI Journal, 16, 151–159. https://doi.org/10.17179/excli2016-783

Issue

Vol. 16 (2017)

Section

Original articles

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