Strontium-Doped Nickel Oxide Nanoparticles: Synthesis, Characterization, and Cytotoxicity Study in Human Lung Cancer A549 Cells

被引:15
作者
Ahmad, Javed [1 ]
Wahab, Rizwan [1 ]
Siddiqui, Maqsood A. [1 ]
Saquib, Quaiser [1 ,2 ]
Ahmad, Naushad [3 ]
Al-Khedhairy, Abdulaziz A. [1 ,2 ]
机构
[1] King Saud Univ, Coll Sci, Zool Dept, Chair DNA Res, Riyadh 11451, Saudi Arabia
[2] King Saud Univ, Coll Sci, Zool Dept, Riyadh 11451, Saudi Arabia
[3] King Saud Univ, Coll Sci, Dept Chem, Riyadh 11451, Saudi Arabia
关键词
Strontium-doped nickel oxide; SEM; TEM; MTT; NRU; ROS; A549; NIO NANOPARTICLES; NEUTRAL RED; IN-VITRO; EXPOSURE;
D O I
10.1007/s12011-021-02780-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this manuscript, the grown and annealed strontium-doped nickel oxide nanoparticles (SrNiONPs) were synthesized using a precipitation method with nickel nitrate and strontium nitrate as precursor agents with trisodium citrate. Various characterization techniques, including X-ray diffraction pattern (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier transform infrared spectroscopy (FTIR), UV-visible, and zeta sizer, were used to thoroughly examine the samples. The XRD pattern (21 nm) was used to calculate the size, phases, and crystallinity of the material (SrNiONPs). In addition to characterization, the material was tested for cytotoxicity in lung cancer cells (A549). The viability test in A549 cells was performed using [3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide] (MTT) and Neutral Red Uptake (NRU) assay with SrNiONPs concentration ranging from 1 to 100 mu g/mL. According to the MTT and NRU data, the toxicity studies are dose-dependent. SrNiONPs also increased reactive oxygen species (ROS) and were involved in apoptosis (A549 cells). Furthermore, quantitative PCR (qPCR) data revealed that the mRNA levels of apoptotic genes marker like p53, bax, and caspase-3 were upregulated, whereas bcl-2, an anti-apoptotic gene, was downregulated. As a result, apoptosis was mediated by the p53, bax, caspase3, and bcl-2 pathways, implying a potential mechanism by which SrNiONPs mediate their toxicity.
引用
收藏
页码:1598 / 1607
页数:10
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