0000000000855647

AUTHOR

Amalia M. Dolga

0000-0001-5400-5614

showing 2 related works from this author

The role of Ca(2+) in cell death caused by oxidative glutamate toxicity and ferroptosis

2018

Ca(2+) ions play a fundamental role in cell death mediated by oxidative glutamate toxicity or oxytosis, a form of programmed cell death similar and possibly identical to other forms of cell death like ferroptosis. Ca(2+) influx from the extracellular space occurs late in a cascade characterized by depletion of the intracellular antioxidant glutathione, increases in cytosolic reactive oxygen species and mitochondrial dysfunction. Here, we aim to compare oxidative glutamate toxicity with ferroptosis, address the signaling pathways that culminate in Ca(2+) influx and cell death and discuss the proteins that mediate this. Recent evidence hints toward a role of the machinery responsible for stor…

0301 basic medicinechemistry.chemical_classificationReactive oxygen speciesProgrammed cell deathPhysiologyGlutamate receptorSTIM1Cell BiologyGlutathioneReviewMitochondrionBiologymedicine.disease_causeCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biologychemistrymedicineJournal ArticleMolecular BiologyIntracellularOxidative stressCell calcium
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Bcl-xL knockout attenuates mitochondrial respiration and causes oxidative stress that is compensated by pentose phosphate pathway activity

2017

Bcl-xL is an anti-apoptotic protein that localizes to the outer mitochondrial membrane and influences mitochondrial bioenergetics by controlling Ca2+ influx into mitochondria. Here, we analyzed the effect of mitochondrial Bcl-xL on mitochondrial shape and function in knockout (KO), wild type and rescued mouse embryonic fibroblast cell lines. Mitochondria of KO cells were more fragmented, exhibited a reduced ATP concentration, and reduced oxidative phosphorylation (OXPHOS) suggesting an increased importance of ATP generation by other means. Under steady-state conditions, acidification of the growth medium as a readout for glycolysis was similar, but upon inhibition of ATP synthase with oligo…

0301 basic medicineOligomycinBioenergeticsOxidative phosphorylationBH4 DOMAINMitochondrionPentose phosphate pathwaymedicine.disease_causeBiochemistryCYTOCHROME-C03 medical and health scienceschemistry.chemical_compoundCHANNEL VDAC0302 clinical medicinePhysiology (medical)BCL-XLmedicineJournal ArticleGlycolysisRELEASEATP synthasebiologyGLUCOSE-METABOLISMFISSIONAPOPTOSIS030104 developmental biologyBiochemistrychemistryCELLSbiology.proteinMEMBRANE030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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