Biologia, Bratislava, 55/Suppl. 8: 45-48, 2000.

ISSN 0006-3088 (Biologia). ISSN 1335-6399 (Biologia. Section Cellular and Molecular Biology).

 

Full Paper

Inhibition of PMN leukocyte chemiluminescence by blood platelets - biological protection against destructive effects of reactive oxygen species?

 

Viera Jancinova*, Radomir Nosal & Katarina Drabikova

Institute of Experimental Pharmacology, Slovak Academy of Sciences, Dubravska cesta 9, SK-84216 Bratislava, Slovakia; fax: +421 7 5477 5928, e-mail: exfavega@savba.sk

* corresponding author

Received: July 10, 2000 / Accepted: October 24, 2000

 

Abstract

Reactive oxygen species produced by polymorphonuclear leukocytes (PMNL) participate substantially in the vascular injury induced by ischaemia and reperfusion. However, clinical observations have indicated that their production was lowered if PMNL interacted with blood platelets. Therefore in this study the effect of platelets on PMNL derived oxidants was analysed using a chemiluminescence method. Co-incubation of isolated human PMNL with platelets (in the cell ratio 1:50 for 6 min at 37C and stirring at 1000 rpm) resulted in 47% inhibition of luminol enhanced chemiluminescence stimulated with Ca2+-ionophore A23187. Platelets were found to be capable of decreasing both extra- and intracellular components of the chemiluminescence signal, i.e. oxygen metabolites produced on the plasma membrane as well as on membranes of intracellular granules. The inhibitory effect of platelets was not abolished by increased concentration of extracellular peroxidase (in the presence of either cytochalasin B or of horse radish peroxidase) and it was evident also in chemiluminescence enhanced with isoluminol, with the concentration of superoxide anion measured selectively. The presented results were indicative of the ability of platelets to decrease the concentration of reactive oxygen species produced by PMNL. As in the ischaemic region platelets are accumulated and activated simultaneously with PMNL, they could represent a unique protective mechanism, active only in case of emergency and selectively at sites exposed to toxic effects of reactive oxygen species.

 

Key words: human blood platelets, polymorphonuclear leukocytes, platelet-leukocyte interactions, chemiluminescence, Ca2+-ionophore A23187.