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Male rats were maintained for periods of up to 16 weeks on a fat free diet which was supplemented with either 4% tripalmitin (essential fatty acid [EFA] deficient) or with 4% safflower oil (SAFF, control). Pulmonary alveolar macrophages (PAM) were obtained by lung lavage. PAM from EFA deficient rats had reduced phagocytic activity and capacity. Intracellular killing of ingested yeast was also reduced by EFA deficiency. The activity of acid phosphatase, beta-glucuronidase and cathepsin D from PAM was not altered by dietary treatment. Transmission electron microscopy failed to show any consistent morphologic differences between PAM from EFA deficient and SAFF animals, but did confirm the decreased phagocytosis by PAM from EFA deficient rats. However, scanning electron microscopy did show loss of pseudopodia in PAM from EFA deficient rats. EFA deficiency was demonstrated by analyzing the methyl esters of the fatty aids from the total lipid extract of PAM. The arachidonate content was decreased while the eicosatrienoate content was increased in PAM derived from rats fed the EFA deficient diet. In an effort to elucidate further the mechanism of action of EFA deficiency in impairing phagocytosis by PAM, inhibitors of various reactions which lead to oxygenated derivatives of arachidonate were studied using PAM from chow fed rats. Some of these inhibitors were effective in diminishing phagocytosis. Furthermore, PAM from these preparations when fixed in suspension and examined with scanning electron microscopy showed morphological changes similar to those seen in EFA deficiency. This similarity of surface ultrastructural changes suggests that EFA deficiency may impair phagocytic function of PAM by reducing availability of an oxygenated derivative of arachidonic acid.
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