Home HOME General Physiology and Biophysics 2016 General Physiology and Biophysics Vol.35, No.4, p.451–458, 2016

Journal info


Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
6 times per year

Aims and Scope
Editorial Info
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.35, No.4, p.451–458, 2016

Title: Apoptotic mechanisms of nickel(II) complex with N1-acetylacetone-N4-4-methoxy-salicylidene-S-allyl-thiosemicarbazone on HL60 leukemia cells
Author: Büşra Kaya, Belkis Atasever-Arslan, Zeynep Kalkan, Hazal Gür, Bahri Ülküseven

Abstract: Thiosemicarbozone complexes that have a broad spectrum of biological activity are formed as a result of condensation reaction between thiosemicarbazide [H2N(C=S)-NH-NH2] and carbonyl-containing compounds. A new nickel(II) complex with N1-acetylacetone-N4-4-methoxy-salicylidene-S-allyl-thiosemicarbazone ligand was synthesized and characterized. We studied the antileukemic activity of the Ni(II) thiosemicarbazone compound and assessed their potential for drug development. Specifically, the effects of this Ni(II) thiosemicarbazone compound on intracellular signal nodes and apoptotic pathways were investigated. According to our results, the Ni(II) thiosemicarbazone compound has apoptotic activity against HL60 cells. Moreover, while Ni(II) thiosemicarbazone compound significantly increased levels of p53 and cleaved caspase-3 proteins, it decreased level of Phospho-Akt1 protein in HL60 cells. The Ni(II) thiosemicarbazone compound could induce HL60 cell apoptosis through inhibiting of PI3K/Akt pathway. These results showed that Ni(II) thiosemicarbozone compound might be an antileukemic agent.

Keywords: Thiosemicarbazone — Apoptosis — HL60 human promyelocytic leukemia cell — Signal transduction
Published online: 06-Oct-2016
Year: 2016, Volume: 35, Issue: 4 Page From: 451, Page To: 458
doi:10.4149/gpb_2016006a


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.