Related Experiment Video
Updated: Jun 3, 2026
Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
Published on: September 7, 2012
Profiling of fatty acids released during calcium-induced mitochondrial permeability transition in isolated rabbit
Jason L Blum1, Gilbert R Kinsey, Prashant Monian
1Center for Cell Death, Injury, and Regeneration, Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, Medical University of South Carolina, Charleston, SC 29425, USA.
Abstract:
Increases in intracellular Ca(2+) during cellular stress often lead to the mitochondrial permeability transition (MPT). We examined changes in fatty acids (FAs) released from isolated renal cortical mitochondria subjected to Ca(2+)-induced MPT. Exposing mitochondria to Ca(2+) stimulated mitochondrial swelling and release of FAs such as arachidonic (20:4) and docosahexenoic acids which increased 71% and 32%, respectively, and linoleic (18:2) which decreased 23% compared to controls. Stearic (18:0), oleic (18:1), and linoleic (18:3) acids were unchanged. To elucidate a mechanism for FA release, mitochondria were pre-treated with bromoenolactone (BEL) to inhibit Ca(2+)-independent phospholipase A(2) gamma activity (iPLA(2)γ). BEL blocked Ca(2+)-induced release of arachidonic and behenic (22:0) acids. Finally, four FAs were released in the absence of Ca(2+) in a BEL-sensitive manner, including arachidonic and docosatrienoic acids. Thus, extensive FA release occurs during Ca(2+)-induced MPT, and that mitochondrial iPLA(2)γ maintains mitochondrial arachidonic acid homeostasis under both basal and Ca(2+)-induced stress conditions.
