Blood platelets decrease concentration of reactive oxygen species produced by polymorphonuclear leukocytes

Reactive oxygen species produced by polymorphonuclear leukocytes (PMNL) participate substantially in vascular injury induced by ischaemia and reperfusion. Blood platelets, accumulated simultaneously with PMNL may modulate this process.

To compare effects of resting and completely stimulated platelets on PMNL-derived oxidants.

Autologous human platelets and PMNL were co-incubated in the physiological cell ratio 50:1, and the formation of reactive oxygen species was detected by luminol- and isoluminol-enhanced chemiluminescence methods. To compare effects of platelets at different degrees of their activation, FMLP (selective PMNL stimulus) and Ca2+-ionophore A23187 (activates both PMNL and platelets) were used as chemiluminescence stimuli. The liberation of serotonin from platelets was estimated fluorometrically.

Both stimulated and non-stimulated platelets inhibited PMNL chemiluminescence. However, while the decreasing effect of resting platelets disappeared at increased extracellular peroxidase concentration, the inhibition of chemiluminescence by activated platelets became even more pronounced after the addition of peroxidase and was accompanied by liberation of serotonin. The concentrations of serotonin released from platelets were sufficiently high to inhibit PMNL chemiluminescence.

The obtained data indicate that by interference of platelets with peroxidase liberation from PMNL and the scavenging effect of platelet serotonin, resting and stimulated platelets might be respectively operative in inhibiting chemiluminescence. Since the presence of blood platelets in the proximity of PMNL effectively decreased the concentration of reactive oxygen species, platelets may represent a unique protective mechanism, active only in case of emergency and selectively at sites exposed to toxic effects of reactive oxygen species. (Tab. 1, Fig. 4, Ref. 42.).