title: Bioenergetic profiling of platelet mitochondria during storage: 4°C storage extends platelet mitochondrial function and viability.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: James A
authors.initials: JA
authors.lastname: Bynum
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: M Adam
authors.initials: MA
authors.lastname: Meledeo
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: Todd M
authors.initials: TM
authors.lastname: Getz
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: Armando C
authors.initials: AC
authors.lastname: Rodriguez
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: James K
authors.initials: JK
authors.lastname: Aden
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Cap
authors.affiliation: US Army Institute of Surgical Research, JBSA-Fort Sam Houston, Texas.
authors.forename: Heather F
authors.initials: HF
authors.lastname: Pidcoke
mesh_terms: D001792:Blood Platelets / Q000166:cytology / Q000378:metabolism*; D001793:Blood Preservation; D002470:Cell Survival; D003080:Cold Temperature; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013997:Time Factors
chemical_list: D017382:Reactive Oxygen Species