Fabrication and physicochemical characterization of copper oxide–pyrrhotite nanocomposites for the cytotoxic effects on HepG2 cells and the mechanism

Author:

He Yun12,Huang Hua3,Fan Minyu2,Wang Zhaojiong2,Liu Xiongwei4,Huo Jiege1

Affiliation:

1. Department of Oncology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine , Nanjing 210028 , China

2. Department of Oncology, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine , Changshu 215500 , China

3. Department of Anorectal, Changshu Hospital Affiliated to Nanjing University of Chinese Medicine , Changshu 215500 , China

4. Department of Oncology, Affiliated Jiangyin Hospital of Medical College, Southeast University , Jiangyin 214400 , China

Abstract

Abstract Novel CuO–FeS nanocomposites were synthesized to exert anticancer effects on HepG2 cells. The formation was initially demonstrated using UV–Visible spectrophotometry analysis, which indicated two peaks at 335 and 370 nm. Characteristic Fourier transform infrared spectroscopy peaks for Cu–O and Fe–S bonds were observed at 516, 577 and 619 cm−1 in addition to other notable peaks. The Miller indices correspond to the lattice spacing of monoclinic CuO and FeS as observed by selected area diffraction rings concurrent with the X-ray diffraction observations. The morphology was interpreted by scanning electron microscopy and transmission electron microscopy, indicating a particle size of 110 nm. As per energy-dispersive X-ray spectroscopy analysis, strong peaks for Cu (0.9, 8 and 9 keV), Fe (6–7 keV), O (0.5 keV) and S (2.5 keV) indicated the formation of CuO–FeS blend with no impurities. A mean particle size of 121.9 nm and polydispersity index of 0.150 were displayed by dynamic light scattering analysis and the zeta potential was −29.2 mV. The composites were not toxic to normal 3T3-L1 cells and were not haemolytic even at higher doses. In addition, the stable composites exerted cytotoxic effects on HepG2 cells (IC50 = 250 ± 5.7 μg/mL) and induced cell death by creating a loss in mitochondrial membrane potential and induction of mitochondrial apoptosis in a ROS-independent manner.

Publisher

Walter de Gruyter GmbH

Subject

Surfaces, Coatings and Films,Process Chemistry and Technology,Energy Engineering and Power Technology,Biomaterials,Medicine (miscellaneous),Biotechnology

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