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

Citation
V. Jancinova et al., Inhibition of PMN leukocyte chemiluminescence by blood platelets - biological protection against destructive effects of reactive oxygen species?, BIOLOGIA, 55, 2000, pp. 45-48
Citations number
9
Categorie Soggetti
Biology
Journal title
BIOLOGIA
ISSN journal
00063088 → ACNP
Volume
55
Year of publication
2000
Supplement
8
Pages
45 - 48
Database
ISI
SICI code
0006-3088(2000)55:<45:IOPLCB>2.0.ZU;2-1
Abstract
Reactive oxygen species produced by polymorphonuclear leukocytes (PMNL) par ticipate substantially in the vascular injury induced by ischaemia and repe rfusion. However, clinical observations have indicated that their productio n was lowered if PMNL interacted with blood platelets. Therefore in this st udy the effect of platelets on PMNL derived oxidants was analysed using a c hemiluminescence method. Co-incubation of isolated human PMNL with platelet s (in the cell ratio 1:50 for 6 min at 37 degreesC and stirring at 1000 rpm ) resulted in 47% inhibition of luminol enhanced chemiluminescence stimulat ed with Ca2+-ionophore A23187. Platelets were found to be capable of decrea sing both extra- and intracellular components of the chemiluminescence sign al i.e, oxygen metabolites produced on the plasma membrane as well as on me mbranes of intracellular granules. The inhibitory effect of platelets was n or abolished by increased concentration of extracellular peroxidase (in the presence of either cytochalasin B or of horse radish peroxidase) and it wa s evident also in chemiluminescence enhanced with isoluminol, with the conc entration of superoxide anion measured selectively. The presented results w ere indicative of the ability of platelets to decrease the concentration of reactive oxygen species produced by PMNL. As in the ischaemic region plate lets are accumulated and activated simultaneously with PMNL, they could rep resent a unique protective mechanism, active only in case of emergency and selectively st sites exposed to toxic effects of reactive oxygen species.