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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Singlet oxygen (1O(2)) disrupts platelet aggregates.

INTRODUCTION: Important mediators of activated polymorphonuclear leukocytes (PMN) are the oxidants HOCl and chloramine, which generate the nonradical photon-emitting oxidant singlet oxygen (1O(2)). Since 1O(2) inhibits platelet aggregation, we became interested in a possible oxidant mediated reversibility of platelet aggregation. METHODS: Chloramine T ( CT) is a stable 1O(2) generator that mimics the natural chloramine N-chloro-taurine. Platelet-rich plasma ( PRP) was incubated with CT 0-8 min after addition of the aggregation agonist (10 microM adenosine-5'-diphosphate, ADP, or 5 microg/ml collagen) and the aggregation was monitored. Platelet function was also analyzed by the platelet function analyzer, PFA-100. Fifty microliters of 200 micromol/l ADP was added to 400 microl PRP. After 1 min at 37 degrees C, 50 microl of 0 or 30 mmol/l CT was added, and after an incubation for 3 min at 37 degrees C, 50 microl of 25% glutaraldehyde was added. The samples were analyzed in a transmission microscope at x3000 and x7000 magnification. RESULTS: Chloramines inhibit platelet function in PRP: about 1 mM CT suppresses 50% of the aggregatory capacity of thrombocytes in normal PRP (effective dose 50%, ED(50)=1 mM chloramine), which is identical to the ED(50) for CT in whole blood. The ADP- or collagen-induced platelet aggregation can be reversed by addition of CT: up to 2 min after the addition of ADP as the aggregation inducer, the aggregation is reversible to more than 70% by addition of a 1O(2) release-inducer (3 mM CT). In contrast, addition of CT 8 min after the addition of ADP results only in about 50% reversal of platelet aggregation. The electron microscopic images of platelets before ADP, after incubation for 4 min at 20 micromol/l ADP, after incubation for 1 min at 20 micromol/l ADP, and a further incubation for 3 min at 3 mmol/l CT demonstrate an ADP-dependent formation of platelet aggregates, which are disrupted by 1O(2) into the single platelets; a phenomenon comparable to the decomposition of a puzzle or the continental drift of the major earth plates. The morphology of oxidized and unoxidized platelets is similar. CONCLUSION: This study demonstrates that 1O(2) inhibits and reverses platelet aggregation. The physiologic signal action and the direct anticoagulant action of 1O(2) might be a new principle for pharmacologic intervention in atherothrombosis.[1]

References

  1. Singlet oxygen (1O(2)) disrupts platelet aggregates. Stief, T.W., Feek, U., Ramaswamy, A., Kretschmer, V., Renz, H., Fareed, J. Thromb. Res. (2001) [Pubmed]
 
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