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Bioenergetic profiling of platelet mitochondria during storage: 4°C storage extends platelet mitochondrial function and viability
Author(s) -
Bynum James A.,
Adam Meledeo M.,
Getz Todd M.,
Rodriguez Armando C.,
Aden James K.,
Cap Andrew P.,
Pidcoke Heather F.
Publication year - 2016
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/trf.13337
Subject(s) - mitochondrion , reactive oxygen species , cold storage , mitochondrial ros , platelet , chemistry , respirometry , andrology , bioenergetics , biochemistry , biology , immunology , medicine , horticulture
BACKGROUND Platelets (PLTs) are stored at room temperature (RT) to preserve in vivo circulation time, but PLT quality is degraded. The PLT storage lesion is mitigated by refrigeration, but questions remain regarding effects of cold storage (4°C) on mitochondrial function. Mitochondrial reactive oxygen species (ROS) generation may adversely affect PLT function and viability during storage, and refrigeration may mitigate these effects. STUDY DESIGN AND METHODS PLTs were stored under two temperature conditions (RT, 20‐24°C; or 4°C, 1‐6°C) and four storage durations (baseline [BL] and Days 3, 5, and 7). Mitochondrial respiration and maximal oxygen utilization were assessed with high‐resolution respirometry. Mitochondrial ROS generation was assessed using a superoxide stain. Rotational thromboelastometry (ROTEM) was performed at BL and on Day 5 to assess PLT function. Collagen‐induced PLT aggregation was measured by impedance aggregometry. RESULTS Mitochondrial ROS in 4°C‐stored samples were lower compared to RT and retained a greater capacity to generate ROS after activation. Mitochondrial respiration and maximal mitochondrial utilization was conserved in PLTs stored at 4°C. ROTEM data demonstrated that net maximum clot firmness was higher in 4°C samples compared to RT and prevented fibrinolysis. The aggregation response to collagen was preserved in the 4°C samples versus RT‐stored PLTs. Aggregation impairment correlated well with attenuated mitochondrial respiration and elevated production of intracellular mitochondrial ROS in the RT PLTs. CONCLUSION Mitochondrial damage and ROS production may contribute to loss of PLT viability during storage, whereas cold storage is known to preserve PLT function. Here we demonstrate that 4°C storage results in less oxidant stress and preserves mitochondrial function and potential compared to RT.