title: Cell integrity and mitochondrial function after Mirasol-PRT treatment for pathogen reduction of apheresis-derived platelets: Results of a three-arm in vitro study.
abstract: BACKGROUND
  Mirasol pathogen reduction technology (PRT) treatment uses riboflavin (vitamin B(2)) in combination with ultraviolet light (UV) to inactivate pathogens in platelet concentrates (PCs). This treatment has been reported to increase glycolytic flux, which could result from damage to mitochondria and/or increased ATP demand.
  
  
  METHODS
  Triple-dose PCs were collected by the Trima Accel device. Immediately after splitting, single units were designated to Mirasol-PRT treatment (M), gamma irradiation (X) or remained untreated (C). Platelet (PLT) mitochondrial transmembrane potential (Deltapsi) was evaluated (JC-1 assay) as well as mitochondrial enzymatic activity (MTS assay). LDH release, p selectin expression, glucose/oxygen consumption and lactate production rates were quantified and compared among study groups during 7days of storage.
  
  
  RESULTS
  Immediately after PRT treatment, no significant changes were found in JC-1 signal, MTS activity, and LDH release indicating that PRT treatment did not alter functional/structural cell or mitochondrial integrity as evidenced by LDH release comparable to untreated study groups. In parallel to significantly higher p selectin expression, treated PLTs exhibited significantly accelerated oxygen and glucose consumption rates associated with increased acidity due to higher lactate production rates throughout storage. Despite larger cell populations with depolarized Deltapsi particularly at days 5 and 7, mitochondrial reduction activity of M units as measured by the MTS assay was maintained and appeared to be up-regulated relative to untreated and irradiated controls.
  
  
  CONCLUSIONS
  Mirasol-PRT treated PLTs increased both glycolytic flux as well as respiratory/enzymatic mitochondrial activity. An increased demand for ATP due to increased alpha granule degranulation may be the driving force for these observations.
authors.affiliation: Transfusion Medicine, University of Cologne, 50937 Cologne, Germany. susanne.picker@uk-koeln.de
authors.forename: Susanne M
authors.initials: SM
authors.lastname: Picker
authors.forename: Alexander
authors.initials: A
authors.lastname: Steisel
authors.forename: Birgit S
authors.initials: BS
authors.lastname: Gathof
mesh_terms: D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D001793:Blood Preservation / Q000009:adverse effects* / Q000379:methods; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D017319:Photosensitizing Agents / Q000009:adverse effects*; D017713:Platelet Transfusion; D010983:Plateletpheresis; D012256:Riboflavin / Q000009:adverse effects*; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D017319:Photosensitizing Agents; D012256:Riboflavin