| Justification: The lungs are constantly exposed to oxidative stress and inflammation which increase the risk of lung damage. Omega-3 polyunsaturated fatty acids (n-3 PUFAs), found in different dietary sources, regulate the expression of various genes involved in eicosanoid production and oxidative stability.;Objective: to determine whether providing different sources of n-3 PUFAs will affect the fatty acid composition, inflammation and oxidation in the lungs of growing rats.;Methods: Growing (age 28 d) Sprague-Dawley rats were randomly assigned (n=10/group) to diets consisting of either corn oil (CO) or n-3 PUFA rich flaxseed (FO), krill (KO), salmon (SO) or tuna (TO) oil for 8 weeks. Diet and tissue fatty acid composition was analyzed by gas chromatography. The enzymes involved in eicosanoid synthesis, 5-lipoxygenase (5-LOX) and cyclooxygenase II (COX II), and the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase 1 (SOD1), were determined using real-time polymerase chain reaction.;Results: Rats fed FO, with the highest alpha-linolenic acid (ALA, 18:2n-3) content, had the highest (P<0.001) lung ALA deposition. Rats fed KO, with the highest eicosapentaenoic acid (EPA, 20:5n3) content, had the highest (P<0.001) lung EPA deposition compared to all diet groups, except SO-fed rats. Rats fed TO, with the highest docosahexaenoic acid (DHA, 22:6n-3) content, had the highest (P<0.001) lung DHA deposition compared to rats fed CO or FO. The relative expression of 5-LOX was significantly up-regulated (P=0.007) in rats fed FO compared to CO-fed rats. Expression of the antioxidant defense enzyme, SOD1 was down-regulated (P=0.01) in TO-fed rats compared to rats fed CO. Dietary TO has an EPA/DHA ratio of 1:2 and had a higher ( P<0.001) lung DHA content compared to rats fed CO.;Significance: The fatty acid composition of the lungs reflected dietary intake. The increase in o-3 PUFAs in lung tissue may affect the risk of lung damage, and in turn, susceptibility to lung diseases by altering gene expression of inflammation and oxidative stability. |
