Platelet glycolytic flux increases stimulated by ultraviolet-induced stress is not the direct cause of platelet morphology and activation changes: possible implications for the role of glucose in platelet storage.

Background: Stress-enhanced platelet (PLT) storage lesions include increased glycolysis, discoid-to-sphere morphology change, and spontaneous PLT activation. It is not clear if reduction in glycolysis can alleviate storage lesion development.

Study Design And Methods: Apheresis PLT concentrates were exposed to 17.2 J/mL UV light and 50 microM riboflavin, followed by storage with various concentrations of 2-deoxyglucose (2-DOG) for 5 days. The control had no UV or 2-DOG exposure.

Results: Lactate production and glucose consumption were increased significantly to 0.1371 +/- 0.0281 and 0.0724 +/- 0.0151 mmol per 10(12) cells per hour for UV-treated PLTs, respectively, when compared to control samples. UV treatment induced a decline in pH to 6.55 +/- 0.26 for treated PLTs on Day 5, hypotonic shock response (HSR) 33 +/- 25 percent, extent of shape change (ESC) to 3.8 +/- 3.6 percent, swirl 1.0 +/- 1.0 and increased P-selectin expression 85.2 +/- 9.4 percent. Addition of 2-DOG up to 20 mmol per L significantly reduced lactate production to 0.0515 +/- 0.0045 mmol per 10(12) cells per hour (p < 0.05) and glucose consumption to 0.0293 +/- 0.0060 mmol per 10(12) cells per hour and increased pH to 7.35 +/- 0.09 in a dose-dependent manner. 2-DOG, however, had no effects on HSR, ESC, swirl, and P-selectin expression. Furthermore, an exaggeration of UV-stressed PLT aggregation by addition of 2-DOG was also observed.

Conclusions: Increased glycolytic flux is not a direct cause for PLT morphology change and spontaneous activation during storage lesion development. Reduction of glucose utilization may increase PLT loss during storage.