When the concentrations were higher than 2.0 mM, a slight decrease in cell survival rates was detected.
This significant decrease in cell survival fraction could be due to the six- to sevenfold increase in GNP accumulation with the surface modification.
The progressive decrease in cell survival induced by cell stretch at 24 and 120 h was also abolished by HCA (Fig. 2d).
The decrease in cell survival induced by cell stretch was also abolished by acidosis both HCA and MA but BHC was ineffective (Fig. 5d).
Cationic particles showed to induce the strongest decrease in cell survival rates of BT-20 cells (0 ± 0 after incubation for 72 h) for a concentration of 20 ng/cell.
As shown in Fig. 2a, the cells incubated with GNP-RGDs prior to the radiation had a 19 ± 6% decrease in cell survival fraction compared to the control cells (with no GNPs).
Unusual cell shape and lack of cell spreading can cause cell death in each of the cell types studied here [36], which may explain the observed decrease in cell survival and proliferation rate of TNAs.
Cancer cells internalized with the GNP drug complex had a 32 ± 9% decrease in cell survival and statistically significant enhancement in DNA (deoxyribonucleic acid) damage as compared to control cells (irradiated with no GNPs) after receiving a radiation dose of 2 Gy with 6 MV photons.
The cells treated with GNP-RGD-BLM and radiation (referred to as IR GNP-RGD-BLM) had a 32 ± 9% (p < 0.05) decrease in cell survival compared to the cells treated with free bleomycin and radiation (referred to as IR BLM), with the survival fraction of 0.13 ± 0.005 and 0.19 ± 0.015, respectively, as shown in Fig. 4a.
TNF-α evoked a dose-dependent decrease in cell survival starting with a concentration of 10 ng/ml (Figure 1A).
The incubation of U937 with TNFα in serum-starved suspension conditions induced a 44%±3 (p<0.01) decrease in cell survival (Fig. 5A).
