The Pasteur effect in human platelets: implications for storage and metabolic control

The Pasteur effect and the associated acidosis have long been considered a major cause of platelet death during storage. We have investigated this phenomenon using a defined platelet preparation and a system whereby the oxidative and glycolytic contributions to total ATP production can be measured over a range of oxygen concentrations from saturating (pO 2 =158 mmHg) to anoxic (pO 2 =0 nmmHg). Platelets do not show a Pasteur effect until the pO 2 decreases to < 2.0 mmHg, whereupon lactate production increases 1.5-fold. The Pasteur effect is therefore not a likely cause of platelet death during storage where pO 2 in a storage bag typically drops to no less than 50 mmHg. The data also have implications for the role of oxygen diffusion in oxidative metabolism, and for the compensatory nature of the Pasteur effect. As platelets are relatively small cells, and the onset of the Pasteur effect occurs at a relatively low oxygen concentration, diffusion may limit the rate of oxygen consumption in most other (larger) cells. The Pasteur effect is only fully compensative if the P/O 2 ratio used for the calculations is lower than the conventional one. Since recent research strongly suggests that the conventional P/O 2 ratio is too high, examples of fully compensative Pasteur effects may be more common than the literature suggests.