Thromb Haemost 1981; 45(02): 116-120
DOI: 10.1055/s-0038-1650146
Original Article
Schattauer GmbH Stuttgart

Modification of Platelet Function by Radical Species Produced During Irradiation of Oxygenated Water

Norman I Krinsky
1)   The Department of Biochemistry and Pharmacology, Tufts University School of Medicine, Boston, MA, U.S.A.
,
Danielle G Sladdin
2)   The Blood Research Laboratory and Medical Division, The Memorial Hospital and the Department of Medicine, University of Massachusetts Medical School, Worcester, MA, U.S.A.
,
Peter H Levine
2)   The Blood Research Laboratory and Medical Division, The Memorial Hospital and the Department of Medicine, University of Massachusetts Medical School, Worcester, MA, U.S.A.
,
Irwin A Taub
3)   Food Engineering Laboratory, U.S. Army Natick Research and Development Command, Natick, MA, U.S.A.
,
Michael G Simic
3)   Food Engineering Laboratory, U.S. Army Natick Research and Development Command, Natick, MA, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 08 April 1980

Accepted 15 January 1981

Publication Date:
05 July 2018 (online)

Summary

Gel-filtered platelets in neutral, oxygen-containing solutions irradiated to a dose of 10 krad with γ-rays display a significant inhibition of ADP-induced aggregation. Though the superoxide anion radical (O- 2) and H2O2 are generated in water irradiated under these conditions, only catalase, but not superoxide dismutase (SOD), conveyed protection against this inhibition of platelet function. When the platelets are in the presence of 10-3 M sodium formate, which converts the majority of the radical species formed to O- 2, inhibition of aggregation was again observed. Under these circumstances, the addition of catalase significantly decreased this inhibition, whereas the addition of SOD was without effect.

In order to separate the platelet-inhibition effects of the radical species generated in the medium from a direct effect of irradiation on platelet components, relatively stable quantities of O- 2. were produced in alkaline solutions and reacted with gel-filtered platelets. Again, an inhibition of ADP-induced aggregation was observed. This inhibition was not significantly altered by the addition of SOD, but was abolished by the addition of catalase, either with or without SOD.

Our observation would indicate that O- 2.is without direct effect on platelet function, but serves as the precursor of H2O2, which can inhibit platelet reactions.

 
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