Quantitation of platelet-activating factor (PAF) in human saliva samples by radioimmunoassay indicated there was, at times, sufficient PAF present to aggregate platelets. However, in certain samples, we observed little or no aggregation, and furthermore, these samples were found to inhibit aggregation induced by PAF (200 pg). Chromatographic fractionation of pooled saliva increased the PAF activity 4-fold, and the observed inhibitory activity was found to co-migrate with the fatty acids. The inhibitory fraction was found to be active against platelet aggregation induced by arachidonic acid (3.4 nmole) as well as PAF (25 pg), but not thrombin (20 mU). These results indicate the existence of a PAF inhibitor in saliva, which may explain why potentially toxic levels of PAF can occur in the saliva of normal, healthy individuals. These findings also highlight an important advantage of the radioimmunoassay over platelet aggregation for the quantitation of PAF in, at least, some biological fluids.
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