Albumin interferes with arachidonate metabolism in platelets and neutrophils.

The in vitro effects of albumin (150-600 microM) on arachidonate metabolism are compared in two types of circulating cells, platelets and neutrophils. The effect of this plasma protein on a functional aspect common to both these blood components, i.e. aggregation, was also investigated. Bovine serum albumin (BSA) significantly inhibited thromboxane B2 formation by washed platelets stimulated with threshold concentrations of collagen. In addition, this protein profoundly affected the formation of the major products via the lipoxygenase pathways, i.e., 12-hydroxyeicosatetraenoic acid and leukotriene B4 by platelets and neutrophils, respectively. This inhibitory effect was also confirmed for both types of cells considered on aggregation. Albumins of human origin and human plasma behaved similarly to BSA on the above parameters. Although the mechanism(s) responsible for the described effects require(s) additional studies, albumin, affecting platelet and neutrophil arachidonate metabolism, as well as the aggregatory response, might influence, in some conditions, cell activation.