Antioxidant defense system is altered by dietary oxidized lipid in first-feeding rainbow trout (Oncorhynchus mykiss).

Abstract: High concentrations of n−3 polyunsaturated fatty acids (PUFA) that are readily susceptible to lipid peroxidative damage are found in fish feeds and in the tissues of fish, especially in early developmental stages. A dietary phospholipid (PL) supply has been shown to be beneficial during these critical stages. The objective of the study was to characterize the response of the antioxidant defense system under dietary prooxidant conditions in presence or absence of dietary PL during early development of rainbow trout. Rainbow trout (Oncorhynchus mykiss) at the first-feeding fry stage (mean weight: 66±2mg) or at the fingerling stage (mean weight: 1.5±0.4g) were fed 4 semi-purified diets supplemented with 12% fresh fish oil or 12% oxidized fish oil and 6% soybean lecithin or 6% soybean oil for 4weeks at 17°C. At fry stages, rainbow trout fry fed the PL-supplemented diets had a significantly higher final body weight than fry fed the PL-free diets (0.37±0.07 vs. 0.27±0.03g, respectively). Dietary inclusion of oxidized lipid reduced growth (0.19±0.02 vs. 0.45±0.07 and 2.5±0.6 vs. 4.8±0.6g, respectively) and increased the mRNA expression of antioxidant enzymes such as glutathione reductase and glutathione S-transferase at both developmental stages. However, dietary control of antioxidant enzyme activities and vitamins was low in rainbow trout fry whereas increased activities of antioxidant enzymes and decreased tocopherol contents were noticed in rainbow trout fingerlings fed oxidized lipid compared to rainbow trout fry fed fresh oil. This resulted in higher content of lipid peroxidation products in rainbow trout fry fed oxidized lipid compared to fish fed fresh lipid whereas this difference was reduced at the fingerling stage. The present study demonstrates that rainbow trout fry are more susceptible to oxidative stress induced by dietary oxidized lipid than rainbow trout fingerlings, possibly due to delayed response or lack of complete development of endogenous antioxidant defense system. [Copyright &y& Elsevier]