Franciso 2007 Eur J Pharmacol: Difference between revisions
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|organism=Human | |organism=Human | ||
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|preparations=Intact cells | |preparations=Intact cells | ||
|enzymes=Complex V;ATP synthase | |enzymes=Complex V;ATP synthase |
Latest revision as of 16:12, 9 November 2016
Franciso R, Perez-Tomas R, Gimenez-Bonafe P, Soto-Cerrato V, Gimenez-Xavier P, Santiago A (2007) Mechanisms of prodigiosin cytotoxicity in human neuroblastoma cell lines. Eur J Pharmacol 572:111-9. |
ยป [[Has info::PMID: 17678643]]
Franciso R, Perez-Tomas R, Gimenez-Bonafe P, Soto-Cerrato V, Gimenez-Xavier P, Santiago A (2007) Eur J Pharmacol
Abstract: Prodigiosin is a bacterial red pigment with cytotoxic properties and potential antitumor activity that has been tested against different cancerous cells. In this study we report the effect and mechanisms of action of prodigiosin against different human neuroblastoma cell lines: SH-SY5Y, LAN-1, IMR-32 (N-type) and SK-N-AS (S-type). We compare the anticancerous effect of prodigiosin with that of cisplatin at different concentrations during 24 h of exposure. Prodigiosin is more potent, with IC50 values lower than 1.5 ฮผM in N-type neuroblastoma cells and around 7 ฮผM in the S-type neuroblastoma cell line. We describe prodigiosin as a proton sequestering agent that destroys the intracellular pH gradient, and propose that its main cytotoxic effect could be related to its action on mitochondria, where it exerts an uncoupling effect on the electronic chain transport of protons to mitochondrial ATP synthase. As a result of this action, ATP production is reduced but without decreasing in oxygen consumption. This mechanism of action differs from those induced by conventional chemotherapeutic drugs, suggesting a possible role for prodigiosin to enhance the effect of antitumor agents in the treatment of neuroblastoma. โข Keywords: Neuroblastoma, Prodigiosin, Cisplatin, Apoptosis
Labels: MiParea: Respiration, Pharmacology;toxicology
Organism: Human
Tissue;cell: Neuroblastoma
Preparation: Intact cells
Enzyme: Complex V;ATP synthase
Regulation: ADP, Inhibitor, Oxygen kinetics
Coupling state: ROUTINE
HRR: Oxygraph-2k