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Difference between revisions of "Erikstein 2010 J Cell Biochem"

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|abstract=Mitochondrial bioenergetics and reactive oxygen species (ROS) often play important roles in cellular stress mechanisms. In this study we investigated how these factors are involved in the stress response triggered by resazurin (Alamar Blue) in cultured cancer cells. Resazurin is a redox reactive compound widely used as reporter agent in assays of cell biology (e.g. cell viability and metabolic activity) due to its colorimetric and fluorimetric properties. In order to investigate resazurin-induced stress mechanisms we employed cells affording different metabolic and regulatory phenotypes. In HL-60 and Jurkat leukemia cells resazurin caused mitochondrial disintegration, respiratory dysfunction, reduced proliferation, and cell death. These effects were preceded by a burst of ROS, especially in HL-60 cells which were also more sensitive and contained autophagic vesicles. Studies in Rho(0) cells (devoid of mitochondrial DNA) indicated that the stress response does not depend on the rates of mitochondrial respiration. The anti-proliferative effect of resazurin was confirmed in native acute myelogenous leukemia (AML) blasts. In conclusion, the data suggest that resazurin triggers cellular ROS production and thereby initiates a stress response leading to mitochondrial dysfunction, reduced proliferation, autophagy, and cell degradation. The ability of cells to tolerate this type of stress may be important in toxicity and chemoresistance.
|abstract=Mitochondrial bioenergetics and reactive oxygen species (ROS) often play important roles in cellular stress mechanisms. In this study we investigated how these factors are involved in the stress response triggered by resazurin (Alamar Blue) in cultured cancer cells. Resazurin is a redox reactive compound widely used as reporter agent in assays of cell biology (e.g. cell viability and metabolic activity) due to its colorimetric and fluorimetric properties. In order to investigate resazurin-induced stress mechanisms we employed cells affording different metabolic and regulatory phenotypes. In HL-60 and Jurkat leukemia cells resazurin caused mitochondrial disintegration, respiratory dysfunction, reduced proliferation, and cell death. These effects were preceded by a burst of ROS, especially in HL-60 cells which were also more sensitive and contained autophagic vesicles. Studies in Rho(0) cells (devoid of mitochondrial DNA) indicated that the stress response does not depend on the rates of mitochondrial respiration. The anti-proliferative effect of resazurin was confirmed in native acute myelogenous leukemia (AML) blasts. In conclusion, the data suggest that resazurin triggers cellular ROS production and thereby initiates a stress response leading to mitochondrial dysfunction, reduced proliferation, autophagy, and cell degradation. The ability of cells to tolerate this type of stress may be important in toxicity and chemoresistance.
|keywords=Cellular stress (reactive oxygen species, mitochondrial respiration); Cell fate (autophagy, cell death); Cell proliferation; Resazurin (Alamar Blue)
|keywords=Cellular stress (reactive oxygen species, mitochondrial respiration); Cell fate (autophagy, cell death); Cell proliferation; Resazurin (Alamar Blue)
|editor=[[Gnaiger E]],
|mipnetlab=NO Bergen Tronstad KJ
|mipnetlab=NO Bergen Tronstad KJ
}}
}}
{{Labeling
{{Labeling
|area=Respiration, Pharmacology;toxicology
|injuries=Oxidative stress;RONS
|organism=Human
|organism=Human
|tissues=Blood cells
|preparations=Intact cells
|preparations=Intact cells
|injuries=Oxidative stress;RONS
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=Leukemia,
}}
}}

Latest revision as of 17:21, 31 January 2020

Publications in the MiPMap
Erikstein BS, Hagland HR, Nikolaisen J, Kulawiec M, Singh KK, Gjertsen BT, Tronstad KJ (2010) Cellular stress induced by resazurin leads to autophagy and cell death via production of reactive oxygen species and mitochondrial impairment. J Cell Biochem 111:574-84.

Β» PMID: 20568117 Open Access

Erikstein BS, Hagland HR, Nikolaisen J, Kulawiec M, Singh KK, Gjertsen BT, Tronstad KJ (2010) J Cell Biochem

Abstract: Mitochondrial bioenergetics and reactive oxygen species (ROS) often play important roles in cellular stress mechanisms. In this study we investigated how these factors are involved in the stress response triggered by resazurin (Alamar Blue) in cultured cancer cells. Resazurin is a redox reactive compound widely used as reporter agent in assays of cell biology (e.g. cell viability and metabolic activity) due to its colorimetric and fluorimetric properties. In order to investigate resazurin-induced stress mechanisms we employed cells affording different metabolic and regulatory phenotypes. In HL-60 and Jurkat leukemia cells resazurin caused mitochondrial disintegration, respiratory dysfunction, reduced proliferation, and cell death. These effects were preceded by a burst of ROS, especially in HL-60 cells which were also more sensitive and contained autophagic vesicles. Studies in Rho(0) cells (devoid of mitochondrial DNA) indicated that the stress response does not depend on the rates of mitochondrial respiration. The anti-proliferative effect of resazurin was confirmed in native acute myelogenous leukemia (AML) blasts. In conclusion, the data suggest that resazurin triggers cellular ROS production and thereby initiates a stress response leading to mitochondrial dysfunction, reduced proliferation, autophagy, and cell degradation. The ability of cells to tolerate this type of stress may be important in toxicity and chemoresistance. β€’ Keywords: Cellular stress (reactive oxygen species, mitochondrial respiration); Cell fate (autophagy, cell death); Cell proliferation; Resazurin (Alamar Blue) β€’ Bioblast editor: Gnaiger E β€’ O2k-Network Lab: NO Bergen Tronstad KJ


Labels: MiParea: Respiration, Pharmacology;toxicology 

Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Blood cells  Preparation: Intact cells 



HRR: Oxygraph-2k 

Leukemia