Influence of UV Light (250 nm) on Platelet Activation
Previous investigations have shown that ultraviolet light (UVL) can cause irreversible aggregation in samples of stirred platelet-rich plasma (PRP). The precise mechanisms involved in UVL-induced platelet activation and the aspects of stimulus-activation-contraction secretion coupling involved were not determined. In the present study we have evaluated the response of normal and abnormal platelets to UVL and the influence of various inhibitors on the platelet reaction. UVL (250 nm) stimulated irreversible aggregation and secretion in stirred samples of PRP. Aspirin and Ibuprofen, which block cyclooxygenase and secretion, did not prevent UVL-induced aggregation. Agents that elevate levels of cAMP and free radical scavengers were also ineffective. Only ascorbic acid (5 mM) and EDTA effectively blocked UVL-stimulated platelet clumping. Thrombosthenic platelets lacking glycoproteins Ilb-IIIa were not aggregated by UVL, but afibrinogenemic platelets responded like normal cells. UVL caused the formation of macroaggregates in washed platelet cytoskeletons that did not enter PAGE gels. Electron microscopy revealed no physical changes in unstirred platelets exposed to UVL. Stirring in the presence of UVL caused the development of stickiness, resulting in the aggregation of discoid platelets. Shape change and internal transformation occurred only after aggregates were well established. Results of the studies indicated that extracellular calcium and GPIIb-IIIa were required for UVL-induced aggregation, but thromboxane A2, fibrinogen, and secretion were unnecessary. Inhibition by ascorbic acid suggests that oxidant-induced changes in the membrane leading to changes in the membrane cytoskeleton may underlie platelet activation by UVL.
KeywordsPlatelet Aggregation Platelet Activation Free Radical Scavenger Platelet Reaction Antiplatelet Drug
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