Assessment of a simple, non-toxic alamar blue cell survival assay to monitor tomato cell viability

2001 ◽  
Vol 12 (5) ◽  
pp. 340-346 ◽  
Author(s):  
Heather-Anne Byth ◽  
Bongani I. Mchunu ◽  
Ian A. Dubery ◽  
Liza Bornman
Keyword(s):  
Cell Viability ◽  
Cell Survival ◽  
Alamar Blue ◽  
Blue Cell ◽  
Survival Assay ◽  
Cell Survival Assay

Photofrin as a radiosensitizer in an in vitro cell survival assay

2003 ◽  
Vol 311 (1) ◽  
pp. 98-103 ◽  
Author(s):  
Ulrike Kulka ◽  
Moshe Schaffer ◽  
Axel Siefert ◽  
Pamela M Schaffer ◽  
Astrid Ölsner ◽  
...  
Keyword(s):  
Cell Survival ◽  
Survival Assay ◽  
Cell Survival Assay

Clonogenic Cell Survival Assay

2005 ◽  
pp. 021-028 ◽  
Author(s):  
Anupama Munshi ◽  
Marvette Hobbs ◽  
Raymond E. Meyn
Keyword(s):  
Cell Survival ◽  
Survival Assay ◽  
Clonogenic Cell ◽  
Cell Survival Assay

scholarly journals Microplate Screening for Apoptosis with Antibody to Single-Stranded DNA Distinguishes Anticancer Drugs from Toxic Chemicals

2003 ◽  
Vol 8 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Oskar S. Frankfurt ◽  
Awtar Krishan
Keyword(s):  
Cell Survival ◽  
Anticancer Drugs ◽  
Mtt Assay ◽  
Toxic Chemicals ◽  
Single Stranded Dna ◽  
Toxic Compounds ◽  
Drug Concentrations ◽  
Survival Assay ◽  
Cell Survival Assay

The effect of anticancer drugs and toxic compounds on cultures of human leukemic cells was evaluated by an enzyme-linked immunosorbent assay (Apoptosis ELISA) that uses a monoclonal antibody against single-stranded DNA to quantitate the apoptotic cells. The concentrations of 13 anticancer drugs, which increased Apoptosis ELISA absorbance, were close to the cytotoxic concentrations determined by the long-term cell survival assay. Short-term tetrazolium-based microculture tetrazolium (MTT) assay was significantly less sensitive than the Apoptosis ELISA and the cell survival assay for all anticancer drugs. For 6 drugs, cytotoxic concentrations measured by the MTT assay were at least 1 log higher than the concentrations inducing apoptosis. Importantly, in contrast to the anticancer drugs, 14 toxic chemicals did not increase the Apoptosis ELISA absorbance at cytotoxic concentrations. The difference in apoptosis induction by the anticancer drugs and the toxic chemicals was especially large in cultures treated with drug concentrations 2-fold higher than the IC50 dose. Although all of the anticancer drugs tested induced intense ELISA reaction (mean absorbance 2.0), all toxic chemicals tested did not induce apoptosis. The Apoptosis ELISA assay could have useful applications in drug development as it can distinguish between clinically useful anticancer drugs and toxic compounds, has sensitivity similar to that of the long-term cell survival assay, and provides insight into the mechanism of drug cytotoxicity by differentiating between compounds killing cells by apoptosis and necrosis. ( Journal of Biomolecular Screening 2003:185-190)

scholarly journals EGFRvIII Promotes Cell Survival during Endoplasmic Reticulum Stress through a Reticulocalbin 1-Dependent Mechanism

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1198
Author(s):  
Juliana Gomez ◽  
Zammam Areeb ◽  
Sarah F. Stuart ◽  
Hong P. T. Nguyen ◽  
Lucia Paradiso ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Er Stress ◽  
Cell Survival ◽  
Glioblastoma Cells ◽  
Over Expression ◽  
Stress Markers ◽  
Apoptotic Protein ◽  
Novel Association ◽  
Reduced Activity

Reticulocalbin 1 (RCN1) is an endoplasmic reticulum (ER)-residing protein, involved in promoting cell survival during pathophysiological conditions that lead to ER stress. However, the key upstream receptor tyrosine kinase that regulates RCN1 expression and its potential role in cell survival in the glioblastoma setting have not been determined. Here, we demonstrate that RCN1 expression significantly correlates with poor glioblastoma patient survival. We also demonstrate that glioblastoma cells with expression of EGFRvIII receptor also have high RCN1 expression. Over-expression of wildtype EGFR also correlated with high RCN1 expression, suggesting that EGFR and EGFRvIII regulate RCN1 expression. Importantly, cells that expressed EGFRvIII and subsequently showed high RCN1 expression displayed greater cell viability under ER stress compared to EGFRvIII negative glioblastoma cells. Consistently, we also demonstrated that RCN1 knockdown reduced cell viability and exogenous introduction of RCN1 enhanced cell viability following induction of ER stress. Mechanistically, we demonstrate that the EGFRvIII-RCN1-driven increase in cell survival is due to the inactivation of the ER stress markers ATF4 and ATF6, maintained expression of the anti-apoptotic protein Bcl-2 and reduced activity of caspase 3/7. Our current findings identify that EGFRvIII regulates RCN1 expression and that this novel association promotes cell survival in glioblastoma cells during ER stress.

scholarly journals Comparison of Linear Poly Ethylene Imine (LPEI) and Poly L-Lysine (PLL) in Fabrication of CHOK1 Cell-Loaded Multilayer Alginate Microcapsules

2020 ◽  
Vol 10 (2) ◽  
pp. 290-296
Author(s):  
Fariba Hajifathaliha ◽  
Arash Mahboubi ◽  
Elham Mohit ◽  
Noushin Bolourchian ◽  
Vahid Khalaj ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Survival ◽  
Metabolic Activity ◽  
Encapsulation Efficiency ◽  
Cell Encapsulation ◽  
High Price ◽  
Ethylene Imine ◽  
Linear Poly ◽  
Cellular Metabolic Activity ◽  
Poly Ethylene

Purpose: Poly l-lysine (PLL) has been introduced as a strengthening covering layer for alginate microcapsules which are the most convenient way for cell encapsulation. Some disadvantages of PLL such as high price and low biocompatibility have prompted scientists to find better alternatives. Linear poly ethylene imine (LPEI), thanks to its highly similar structure to PLL, could be considered as a proper cost-effective alternative. In this study LPEI and PLL were compared as covering layers of cell-loaded alginate-LPEI-alginate (cALA) and alginate-PLL-alginate (cAPA) microcapsules. Methods: In addition to the physico-mechanical properties, the encapsulation efficiency, cell survival post encapsulation, cell viability, and cellular metabolic activity within the microcapsules were evaluated using trypan blue, live/dead cell staining, and MTT test, respectively. Results: Physico-mechanical evaluation of the microcapsules revealed that the cell microencapsulation process did not affect their shape, size, and mechanical stability. Although the encapsulation efficiency for cALA and cAPA was not different (P>0.05), cell survival post encapsulation was higher in cALA than in cAPA (P<0.05) which could be the reason for the higher cell viability and also cellular metabolic activity within these microcapsules in comparison to cAPA. Conclusion: Here, based on these results, ALA could be introduced as a preferable alternative to APA for cell encapsulation.

Comparison of Effects of Curcumin and Nano-curcumin on the Survival of Human-Derived Mesenchymal Stem Cells: An Experimental Study

2020 ◽  
Vol 11 (2) ◽  
pp. 148-155
Author(s):  
Pinjari Hameeda ◽  
Sandeep Katti ◽  
Rajkishore Jammalamadugu ◽  
Kishore Bhatt ◽  
Malleswara Rao Peram ◽  
...  
Keyword(s):  
Stem Cells ◽  
Experimental Study ◽  
Mesenchymal Stem Cells ◽  
Survival Rate ◽  
Cell Viability ◽  
Cell Survival ◽  
Dependent Manner ◽  
Cell Survival Rate ◽  
Post Hoc ◽  
Dose Dependent

Aim: To evaluate and compare the effect of curcumin (CUR) and Nano-curcumin (N-CUR) on human-derived mesenchymal stem cells (MSCs) in a dose-dependent manner. Materials and Methods: An experimental study performed with putative MSCs from a total of five systemically healthy subjects with chronic periodontitis. These putative MSCs were isolated by cell culture and were further characterized and identified by colony-forming unit assay and immunocytochemical analysis using cell surface markers CD105, CD146, CD45 and CD73. The identified MSCs were treated with different doses of CUR and N-CUR, and compared with α-minimum essential medium (α -MEM) for its cell viability by performing MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay for 48 and 72 hr. The statistically analysis was performed using one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test and Bonferroni’s post hoc test. Results: Compared to the α-MEM group, both CUR and N-CUR treated cells have shown significantly ( P = .029) higher survival rate at lower concentration (0.1 and 0.5 µM/L), at 48 hr incubation. However, there was no statistically significant difference between the CUR and N-CUR groups on cell survival rate at both 48 and 72 hr incubation. When compared between the concentrations of the same group, significantly higher cell viability ( P = .001) was observed at lower concentrations (0.1, 0.5 µM/L) in both test groups after incubation for 48 and 72 hr. Conclusion: Both CUR and N-CUR have a dose-dependent effect on human derived MSCs survival when incubated for 48 hr, whereas N-CUR shows increased cell survival rate even at 72 hr of incubation. Although, the cautious use of CUR and N-CUR at higher concentrations is recommended.

THE EFFECT OF SULPHAEMOGLOBIN ON RED CELL VIABILITY

1957 ◽  
Vol 35 (1) ◽  
pp. 1171-1181
Author(s):  
L. G. Israels ◽  
A. Chutorian ◽  
G. E. Delory ◽  
Esther Israels
Keyword(s):  
Cell Viability ◽  
Life Span ◽  
Cell Survival ◽  
Red Cells ◽  
Red Cell ◽  
Disappearance Rate ◽  
Cell Life ◽  
Red Cell Survival ◽  
Calcium Sulphide ◽  
True Measure

Sulphaemoglobinaemia was produced in rabbits by the injection of para-aminopropriophenone and calcium sulphide. The disappearance of this pigment from the blood was used as an index of red cell survival. Sulphaemoglobin disappeared in an exponential fashion, indicating a mean red cell life span of 36 days. The red cells were also tagged with Cr51, and this method of measuring erythrocyte life span yielded values strongly suggesting that sulphaemoglobin in the red cell impairs its viability and leads to random cell destruction. Under these conditions it would seem that the disappearance rate of sulphaemoglobin is not a true measure of red cell survival.

scholarly journals Nitric Oxide Inhibits Caspase Activation and Apoptotic Morphology but Does Not Rescue Neuronal Death

2005 ◽  
Vol 25 (3) ◽  
pp. 348-357 ◽  
Author(s):  
Ping Zhou ◽  
Liping Qian ◽  
Costantino Iadecola
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Cell Viability ◽  
Cell Survival ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Cysteine Residue ◽  
Caspase Activity ◽  
No Donors ◽  
Apoptotic Morphology

Nitric oxide (NO) has been shown to inhibit apoptotic cell death by S-nitrosylation of the catalytic-site cysteine residue of caspases. However, it is not clear whether in neurons NO-mediated caspase inactivation leads to improved cell survival. To address this issue, we studied the effect of NO donors on caspase activity and cell survival in cortical neuronal culture treated with the apoptosis inducer staurosporine (STS) and camptothecin. In parallel, cell viability was assessed by the MTS assay and MAP2 staining. We found that NO donors ((±)- S-nitroso- N-acetylpenicillamine, S-nitrosoglutathione, and NONOates) dose-dependently inhibited caspase-3 and -9 activity induced by STS and camptothecin. The reduction in caspase-3 activity was, in large part, because of the blockage of the proteolytic conversion of pro-caspase-3 to active caspase-3. NO donors also inhibited the appearance of the classical apoptotic nuclear morphology. However, inhibition of both caspase activity and apoptotic morphology was not associated with enhancement of cell viability. Thus, inhibition of caspase and apoptotic morphology by NO donors does not improve neuronal survival. The data suggest that inhibition of caspase by NO unmasks a caspase-independent form of cell death. A better understanding of this form of cell death may provide new strategies for neuroprotection in neuropathologies, such as ischemic brain injury, associated with apoptosis.

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