Balint J A, Karakashian G V, Beeler D A, Megirian R, Kaye N W
Trans Am Clin Climatol Assoc. 1985;96:67-78.
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.
雄性大鼠在无脂饮食条件下饲养长达16周，该饮食分别补充4%的三棕榈酸甘油酯（缺乏必需脂肪酸[EFA]）或4%的红花油（SAFF，对照）。通过肺灌洗获取肺泡巨噬细胞（PAM）。来自EFA缺乏大鼠的PAM吞噬活性和能力降低。EFA缺乏也会降低对摄入酵母的细胞内杀伤作用。饮食处理未改变PAM中酸性磷酸酶、β-葡萄糖醛酸酶和组织蛋白酶D的活性。透射电子显微镜未能显示EFA缺乏大鼠和SAFF大鼠的PAM之间存在任何一致的形态学差异，但确实证实了EFA缺乏大鼠的PAM吞噬作用降低。然而，扫描电子显微镜显示EFA缺乏大鼠的PAM中伪足缺失。通过分析PAM总脂质提取物中脂肪酸的甲酯来证明EFA缺乏。在喂食EFA缺乏饮食的大鼠来源的PAM中，花生四烯酸含量降低，而二十碳三烯酸含量增加。为了进一步阐明EFA缺乏损害PAM吞噬作用的作用机制，使用来自正常饮食大鼠的PAM研究了导致花生四烯酸氧化衍生物的各种反应的抑制剂。其中一些抑制剂可有效减少吞噬作用。此外，这些制剂中的PAM在悬浮液中固定并用扫描电子显微镜检查时，显示出与EFA缺乏时相似的形态变化。表面超微结构变化的这种相似性表明，EFA缺乏可能通过减少花生四烯酸氧化衍生物的可用性来损害PAM的吞噬功能。
