Prakorn ChudapongseMahidol University2018-04-192018-04-191976-02-16BBA - Bioenergetics. Vol.423, No.2 (1976), 196-202000527282-s2.0-0017225177https://repository.li.mahidol.ac.th/handle/20.500.14594/10841Phosphoenolpyruvate was found to depress extra oxygen consumption associated with Ca 2+ -induced respiratory jump by rat heart mitochondria. Addition of phosphoenolpyruvate to mitochondria which have accumulated Ca 2+ in the presence of glutamate and inorganic phosphate causes the release of Ca 2+ from mitochondria. The phosphoenolpyruvate-stimulated Ca 2+ efflux can be observed with mitochondria loaded with low initial Ca 2+ concentration (0.12 mM) in the incubation medium. Measurements of mitochondrial H + translocation produced by addition of Ca 2+ to respiring mitochondria show that phosphoenolpyruvate depresses H + ejection and enhances H + uptake by mitochondria. The Ca 2+ -releasing effect of phosphoenolpyruvate was found to be significantly stronger than that produced by rotenone when added to mitochondria loaded with Ca 2+ in the presence of glutamate and inorganic phosphate. Dithiothreitol cannot overcome the effect of phosphoenolpyruvate on mitochondrial Ca 2+ transport. © 1976.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineFurther studies on the effect of phosphoenolpyruvate on respiration-dependent calcium transport by rat heart mitochondriaArticleSCOPUS10.1016/0005-2728(76)90178-X