scholarly journals Endocytosis and Lack of Cytotoxicity of Alkyl-Capped Silicon Quantum Dots Prepared from Porous Silicon

Materials ◽  
2019 ◽  
Vol 12 (10) ◽  
pp. 1702 ◽  
Author(s):  
Wipaporn Phatvej ◽  
Harish K. Datta ◽  
Simon C. Wilkinson ◽  
Elaine Mutch ◽  
Ann K. Daly ◽  
...  

Freely-dissolved silicon quantum dots were prepared by thermal hydrosilation of 1-undecene at high-porosity porous silicon under reflux in toluene. This reaction produces a suspension of alkyl-capped silicon quantum dots (alkyl SiQDs) with bright orange luminescence, a core Si nanocrystal diameter of about 2.5 nm and a total particle diameter of about 5 nm. Previous work has shown that these particles are rapidly endocytosed by malignant cell lines and have little or no acute toxicity as judged by the standard 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for viability and the Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay for apoptosis. We have extended this work to the CACO-2 cell line, an established model for the human small intestinal mucosa, and demonstrate that neither acute nor chronic (14 days) toxicity is observed as judged by cell morphology, viability, ATP production, ROS production and DNA damage (single cell gel electrophoresis) at doses of 50–200 μ g mL − 1 . Quantitative assessment of the extent of uptake of alkyl SiQDs by CACO-2, HeLa, HepG2, and Huh7 cell lines by flow cytometry showed a wide variation. The liver cell lines (HepG2 and Huh7) were the most active and HeLa and CACO-2 showed comparable activity. Previous work has reported a cholesterol-sensitivity of the endocytosis (HeLa), which suggests a caveolin-mediated pathway. However, gene expression analysis by quantitative real–time polymerase chain reaction (RT-PCR) indicates very low levels of caveolins 1 and 2 in HepG2 and much higher levels in HeLa. The data suggest that the mechanism of endocytosis of the alkyl SiQDs is cell-line dependent.

1999 ◽  
Vol 82 (1) ◽  
pp. 197-200 ◽  
Author(s):  
M. V. Wolkin ◽  
J. Jorne ◽  
P. M. Fauchet ◽  
G. Allan ◽  
C. Delerue

2002 ◽  
Vol 65 (3) ◽  
Author(s):  
Md. N. Islam ◽  
R. N. Panda ◽  
A. Pradhan ◽  
Satyendra Kumar

2021 ◽  
Vol 258 ◽  
pp. 123935
Author(s):  
Mohammad S. Almomani ◽  
Naser M. Ahmed ◽  
Marzaini Rashid ◽  
M.A. Almessiere ◽  
Abeer S. Altowyan

2020 ◽  
Vol 222 ◽  
pp. 318-331 ◽  
Author(s):  
Maxim B. Gongalsky ◽  
Uliana A. Tsurikova ◽  
Catherine J. Storey ◽  
Yana V. Evstratova ◽  
Andrew A. Kudryavtsev ◽  
...  

Tailoring of the cytotoxicity and dissolution rate of luminescent porous silicon quantum dots is presented.


Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3135
Author(s):  
Dominik Poradowski ◽  
Izabela Janus ◽  
Aleksander Chrószcz ◽  
Bożena Obmińska-Mrukowicz

The study describes the cytotoxic effect against human and canine osteosarcoma (U-2 OS and D-17) cell lines induced by risedronate sodium and meloxicam per se and in combination. Both cell lines were prepared according to standard procedures for cell cultures studies. The cell viability was estimated in both cell lines treated with chosen concentrations of risedronate sodium and meloxicam. The apoptosis assessment was carried out using TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay. EC50 values, computed for risedronate sodium and meloxicam cytotoxicity, showed comparable effects against the canine OS cell line in similar concentration of both drugs. In case of human OS, the stronger cytotoxic effect of risedronate sodium was proved. The EC50 values for meloxicam in both cell lines were, statistically, significantly different (* p < 0.05). Moreover, the cytotoxic effect of a combined administration of meloxicam and risedronate sodium in doses 100 µg/mL, compared with the negative control showed statistically significant differences. The human OS cell line was more resistant to both compounds than the canine OS cell line. The apoptotic effect in canine and human osteosarcoma triggered by risedronate sodium and meloxicam was statistically significant (p < 0.05). The cytotoxic effect induced with 100 µg/mL of risedronate sodium proved statistically significant differences between both tested cell lines compared to negative control. The results obtained with 10 and 100 µg/mL of meloxicam were not statistically significant. The study showed the synergic mechanism of action of risedronate sodium and meloxicam, but the concentrations used in vitro will not be possible to achieve in in vivo. Therefore, our results serve as basis only to design future studies on the tissue level.


APL Materials ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 081105
Author(s):  
Toshihiro Nakamura ◽  
Nobuyoshi Koshida ◽  
Ze Yuan ◽  
Jun Otsubo

2009 ◽  
Vol 58 (7) ◽  
pp. 4652
Author(s):  
Huang Wei-Qi ◽  
Wang Xiao-Yun ◽  
Zhang Rong-Tao ◽  
Yu Shi-Qiang ◽  
Qin Chao-Jian

2021 ◽  
Vol 11 ◽  
Author(s):  
Mahyar Sameti ◽  
Pablo R. Castello ◽  
Matthew Lanoue ◽  
Tatiana Karpova ◽  
Carlos F. Martino

In this study, we characterized the bioenergetic response of the Lund human mesencephalic (LUHMES) cell line and a mouse astrocyte cell line to oxidative stress. Extracellular hydrogen peroxide  (H2O2) levels and bioenergetic response were investigated in these cell lines after exposure to paraquat (PQ), a redox cycling compound that causes oxidative stress in cells. We used extracellular flux analysis to measure mitochondrial function in adherent astrocytes and LUHMES cells. Extracellular H2O2 was measured fluorometrically. H2O2 levels increased in both cell lines after exposure to 5 µM PQ for 18 h; however, the extent of H2O2 increase with astrocytes was significantly lower than that with LUHMES cells (33% vs. 67%). Measurements of basal mitochondrial respiration showed that PQ almost completely eliminated oxygen consumption rate (OCR) in astrocytes and significantly reduced it in LUHMES cells. Notably, OCR in LUHMES cells was higher than that in astrocytes, indicating that neuronal cells maintain higher oxidative metabolism than glial cells, which is also consistent with higher energy demands of the neuronal cells. Moreover, LUHMES cells exhibited a higher amount of adenosine triphosphate (ATP) being produced by oxidative phosphorylation than by glycolysis. In contrast, astrocytes demonstrated a higher glycolytic capacity and glycolytic reserve than LUHMES cells and higher ATP production rate by glycolysis than its production by mitochondrial oxidative metabolism. Collectively, this study showed the differential bioenergetic responses between astrocytes and LUHMES cells in responding to oxidative stress and the findings may provide insights into the mitochondrial reserve capacity in neurons and astrocytes in responding to oxidative stress. (First online: Mar 30, 2021)


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