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Bioflavonoids protect cells against halogenated boroxine-induced genotoxic damage by upregulation of hTERT expression.

Authors :
Hadzic, Maida
Haveric, Sanin
Haveric, Anja
Lojo-Kadric, Naida
Galic, Borivoj
Ramic, Jasmin
Pojskic, Lejla
Source :
Zeitschrift für Naturforschung B: A Journal of Chemical Sciences; May2019, Vol. 74 Issue 5, p125-129, 5p
Publication Year :
2019

Abstract

Plant bioflavonoids are widely present in the human diet and have various protective properties. In this study, we have demonstrated the capacity of delphinidin and luteolin to increase human telomerase reverse transcriptase (hTERT) expression level and act as protective agents against halogenated boroxine-induced genotoxic damage. Halogenated boroxine K<subscript>2</subscript>(B<subscript>3</subscript>O<subscript>3</subscript>F<subscript>4</subscript>OH) (HB), is a novel compound with potential for the treatment of both benign and malignant skin changes. In vivo and in vitro studies have confirmed the inhibitory effects of HB on carcinoma cell proliferation and cell cycle progression as well as enzyme inhibition. However, minor genotoxic effects of HB are registered in higher applied concentrations, but those can be suppressed by in vitro addition of delphinidin and luteolin in appropriate concentrations. Fresh peripheral blood samples were cultivated for 72 h followed by independent and concomitant treatments of HB with luteolin or delphinidin. We analyzed the differences in relative hTERT expression between series of treatments compared with controls, which were based on normalized ratios with housekeeping genes. The obtained results have shown that selected bioflavonoids induce upregulation of hTERT that may contribute to the repair of genotoxic damage in vitro. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09320776
Volume :
74
Issue :
5
Database :
Complementary Index
Journal :
Zeitschrift für Naturforschung B: A Journal of Chemical Sciences
Publication Type :
Academic Journal
Accession number :
138503691
Full Text :
https://doi.org/10.1515/znc-2018-0132