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Measurement and Analysis of the Mitochondrial Calcium Sequestration and Effects on the Buffering System
Author(s) -
Strubbe Jasiel O.,
Zhang Yizhu,
Truong Hai,
Bazil Jason N.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.618.8
Subject(s) - calcium , mitochondrion , calcium signaling , microbiology and biotechnology , bioenergetics , reactive oxygen species , calcium metabolism , oxidative stress , mitochondrial ros , chemistry , oxidative phosphorylation , biology , signal transduction , biochemistry , organic chemistry
Calcium is a key signaling molecule found to regulate many cellular processes, including but not limited to, cellular physiology, bioenergetics, transcriptional events, signal transduction, and reactive oxygen species (ROS) production. While mitochondrial calcium dynamics have been extensively studied, it is yet unclear how calcium is sequestered and buffered in a quantitatively and mechanistic manner. Mitochondrial‐calcium homeostasis plays a crucial role in cell fate by a tightly‐regulated buffering system that maintains sub‐lethal levels of free calcium. If the calcium buffering capacity is exceeded mitochondrial dysfunction can result in excessive ROS production, initiating cell death signaling pathways, and catastrophic energy failure. In this study, we quantitatively characterized the mitochondrial calcium buffering power under a variety of experimental conditions and two calcium loading protocols. This was done with isolated cardiac mitochondria from guinea pigs using calcium‐sensitive molecular dyes. The mitochondrial calcium buffering power was quantified by monitoring the calcium flux from both outside and inside the mitochondria. Here, we report the changes in calcium buffering power caused by oxidative stress and under conditions that promote calcium uptake and retention. Furthermore, we demonstrate that the buffering power is also affected by the way calcium is loaded into the mitochondria. These data provide further insights on the mitochondrial calcium loading capacity and raises the question as to what are the components that regulate free calcium in the system. Support or Funding Information This research is supported by the National Heart, Lung, and Blood Institute (R00‐HL121160). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .