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Our data clearly demonstrate that H2O2 induced a great cell viability lost (by about 40%), in agreement with Chetsawang et al. [ 31] who found SH-SY5Y cells loss viability mediated by H2O2.
The GRANTA-519, UPN-1 and REC-1 cells were resistant to VD3 (>80% of viability at 150 nM), whereas the JEKO-1, MINO and Z-138 cells were weakly sensitive with a maximum of loss viability of 32% for Z-138 cells.
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Addition of ACM resulted in a significant neuroprotective effect against H2O2-induced injury, compared with unconditioned medium (31.0±1.8% loss of viability compared with control: 41.4±1.4% loss of viability; Figure 2c, P<0.05).
Hence, our data show the effects of 20 nM paclitaxel, producing a loss of viability of approximately 25% in MCF-7 and only 8% loss of viability in the paclitaxel-resistant MCF-7TaxR line.
Silencing CASP8 completely blocked the TRAIL-induced loss of viability, whereas silencing FLIP resulted in a significantly greater TRAIL-induced loss of viability.
Seventy-two hours incubation with barasertib-hQPA caused loss of viability in both transporter negative cell lines with an almost complete loss of viability achieved at 30 nM and 2B ii)).
Loss of viability was confirmed by L. monocytogenes counts (cfu/cm2).
The production of malondialdehyde (MDA) was observed during E. coli loss of viability.
This was not associated with any loss in viability determined by trypan blue exclusion (B).
However, for 10% γ-PGA-protected cells, the loss in viability was reduced to 0.51 log CFU/ml.
By increasing the time of incubation, the loss of viability increased after 3 to 4 h of incubation.
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