In the United States, supplemental dietary lipid is typically provided as an animal-vegetable blend using animal tallow or hydrogenated oils from the food industry. Lipids from these sources are rich in saturated, trans, n-6 fatty acids and poor in n-3 fatty acids. Linoleic (18:2 n-6) and alpha-linolenic (18:3 n-3) acids are essential fatty acids and are the precursors of long-chain n-6 and n-3 fatty acids such as arachidonic and eicosapentaenoic acids (EPA). Ester-linked arachidonic acid and EPA can be mobilized by phospholipase A(2) to generate free arachidonic acid and EPA, which can act as substrates for cyclooxygenase and lipooxygenase to produce eicosanoids. Eicosanoids derived from arachidonic acid, prostaglandin E2, thromboxane B2, and leukotriene B4 are proinflammatory and more potent than eicosanoids derived from EPA such as prostaglandin E3, thromboxane B3, and leukotriene B5. Developing dietary strategies in broiler chickens that enhance the n-3 fatty acid content of tissues is also associated with lipid oxidation and muscle product quality. Therefore, alternative strategies for enhancing tissue n-3 fatty acid content without affecting growth and product quality must be devised. The role of maternal (yolk) fatty acids in modulating the long-chain n-3 fatty acid content of tissues and eicosanoid production in chickens fed a diet lacking in long-chain n-3 fatty acids is investigated. Up to d 42 of growth, the cardiac tissues of chicks hatched from hens fed a high n-3 diet retained higher levels of long-chain n-3 fatty acids than those of chicks hatched from hens fed a low n-3 diet. Chicks hatched from hens fed a high n-3 diet produced less proinflammatory eicosanoids than chicks hatched from hens fed a low n-3 diet. Modulating maternal dietary n-3 fatty acids enhances tissue retention of n-3 fatty acids during growth and reduces proinflammatory eicosanoid production in chicks, which could lead to fewer metabolic and inflammatory-related disorders in poultry.