Lead (Pb) affects elements of humoral and cell-mediated immunity, and diminishes host resistance to infectious disease. Evidence is presented supporting a hypothesis of Pb-induced immunosuppression stemming from altered fatty acid metabolism, and mediated by eicosanoids and macrophages (MO). Chronic Pb exposure increases the proportion of arachidonate (ArA) among fatty acids in lipid from avian tissues, and this change provides precursors for eicosanoids, the oxygenated derivatives of ArA that mediate MO acute inflammatory response. In the current study, we showed that the concentration of ArA in phospholipids of MO elicited from turkey poults fed 100 ppm dietary Pb acetate was twice that of controls. In vitro production of eicosanoids by these MO was substantially increased, and this effect was most pronounced following lipopolysaccharide stimulation: prostaglandin F2 alpha was increased 11-fold, thromboxane B2 increased threefold, and prostaglandin E2 increased by 1.5 times. In vitro phagocytic potential of these MO was suppressed, such that the percentage of MO engulfing sheep red blood cell (RBC) targets was reduced to half that of control MO. In vivo susceptibility of Pb-treated and control birds to Gram-negative bacteria challenge was also evaluated. The morbidity of chicks inoculated with Salmonella gallinarum and fed either control or 200 ppm Pb acetate-supplemented diets was similar, except early in the course of the disease when mortality among Pb-treated birds was marginally greater. In these studies, effects of Pb that could influence immunological homeostasis were demonstrated for MO metabolism of ArA, for production of eicosanoids, and for phagocytosis. There was also the suggestion that these in vitro indices of immune function are related to in vivo disease resistance.

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PubMedDate not supplied

Lead toxicity in chickens. Interaction with toxic dietary levels of selenium.

Two experiments were conducted in which varying levels of lead (up to 2000 ppm as lead acetate trihydrate) and selenium (up to 40 ppm as Na2SeO3) were fed, either alone or in combination, to chicks from day-old through 18 or 20 d. Lead additions depressed growth in a dose-dependent manner without affecting mortality. Selenium addition at 20 ppm was severely growth inhibitory, but mortality was not affected. The growth inhibition of 20 ppm Se was partially alleviated by feeding it in combination with 2000 ppm Pb; however, mortality was increased significantly by the combination. In contrast 40 ppm Se resulted in almost complete cessation of growth and 85% mortality, whereas the combination with 2000 ppm Pb partially overcame the growth inhibition and eliminated the excess mortality. When Pb or Se were fed alone, hepatic levels of the fed element were elevated. There were further significant elevations of hepatic levels of both elements when fed in combination at identical dietary concentrations as the single element additions. The results suggest that Pb and Se are antagonistic. The nature of the interaction of these elements is such that although 2000 ppm Pb partially overcomes the growth inhibition by 20 or 40 pm Se, the reverse (relief of Pb inhibition by Se) is not observed.

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PubMedDate not supplied

Influence of diet on a retrovirus-induced obesity and stunting syndrome.

An avian retrovirus, RAV-7, causes a syndrome characterized by stunting, high mortality, and obesity. In this study, the influence of the lipid content of the diet on the RAV-7-induced syndrome was examined. Failure to gain weight, a measure of the stunting, was not influenced by fat content of the diet, but a slight increase in mortality was noted with a low-fat diet.

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