Abstract

Phosphine metal complexes have been recently evaluated in the field of cancer therapy. In this research, the cytotoxic effects of some metal phosphines {[PdCl2((CH2OH)2PCH2)2NCH3] (C1), [RuCl2(((CH2OH)2PCH2)2NCH3)2] (C2), [PtCl2((Ph2PCH2)2NCH3)(timin)2] (C3)} on K562 (human myelogenous leukemia cell line) and A549 (adenocarcinomic human alveolar basal epithelial cells) cells were investigated using the MTT test. C1 and C2 are water-soluble metal complexes, which may have some advantages in in vitro and in vivo studies. The effects of the above-mentioned metal complexes on thioredoxin reductase (TrxR) (EC: 1.8.1.9), glutathione peroxidase (GPx) (EC: 1.11.1.9), and catalase (Cat) (EC: 1.11.1.6) enzymes were also tested. The results of this research showed that all three metal complexes indicated dose-dependent cytotoxicity on A549 and K562 cell lines and that the complexes inhibited different percentages of the TrxR, GPx, and Cat enzymes of these tumor cells.

Highlights

  • Some anticancer agents act through production of ROS to kill tumor cells

  • The cytotoxic activities of Ru(II), Pd(II), and Pt(II) phosphine complexes on A549 and K562 cell lines, and the inactivation of the glutathione peroxidase (GPx), Cat, and thioredoxin reductase (TrxR) enzymes of these cells via the metal phosphine complexes have been investigated in this study

  • The results showed that A549 cells were resistant to death whereas K562 cells have low resistance in the presence of metal complexes

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Summary

Introduction

Some anticancer agents act through production of ROS (reactive oxygen species) to kill tumor cells. Reported studies have shown that cells with high levels of antioxidant enzymes are resistant to some anticancer agents [1, 2]. The inhibition of these enzymes is an indicator of apoptotic pathways, and organometallic compounds have been most recently used as the first step of cancer drug discovery [3,4,5]. The cytotoxic activities of Ru(II), Pd(II), and Pt(II) phosphine complexes on A549 and K562 cell lines, and the inactivation of the GPx, Cat, and TrxR enzymes of these cells via the metal phosphine complexes have been investigated in this study

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