The effects of conjugated linoleic acid (CLA) on growth performance, non-specific immunity, antioxidant capacity, lipid deposition and related gene expression were investigated in the large yellow croaker (Larmichthys crocea). Fish (7·56 (sem 0·60) g) were fed soyabean oil-based diets with graded levels of CLA (0, 0·42, 0·83, 1·70 %) for 70 d. Quantitative PCR was used to assess the effects of CLA on the transcription of inflammation- and fatty acid oxidation-related genes. Growth in fish fed the diet with 0·42 % CLA was significantly higher. Also, phagocytic index and respiratory burst activity were significantly higher in fish fed the diets containing 0·42 and 0·83 % CLA, respectively. Hepatic total antioxidative capacity and catalase activities increased significantly when CLA increased from 0 to 0·83 %, and then decreased with further increase of CLA. However, hepatic malondialdehyde content decreased significantly as dietary CLA increased. Lipid concentration in the whole body and muscle increased significantly with increasing dietary CLA. Transcription of genes related to inflammation (cyclo-oxygenase-2 and IL-β) in the liver and kidney and fatty acid oxidation (carnitine palmitoyl transferase I and acyl CoA oxidase) in the kidney decreased significantly as dietary CLA increased. PPARα and acyl CoA oxidase expression in the liver decreased significantly as CLA increased from 0·42 to 1·70 %. These results strongly suggest that dietary CLA could significantly affect growth performance, non-specific immunity, antioxidant capacity, lipid deposition and transcription of inflammation- and fatty acid oxidation-related genes of the large yellow croaker. This may contribute to our understanding of the mechanisms related to the physiological effects of dietary CLA in fish.

Chronic subcutaneous (s.c.) administration of d-galactose (DG) to BL/6J mice has been shown to induce oxidative stress and is considered a model to mimic accelerated ageing. Fructo-oligosaccharide (FO) is a well-defined prebiotic and its fermentation by lactic acid bacteria has been shown to exert antioxidative capacity. The present study was aimed to determine whether FO attenuated DG-induced oxidative stress and hepatopathy in Balb/cJ mice. Mice (12 weeks of age, n 40) were divided into control (s.c. saline), DG (s.c. 1·2 g/kg body weight), DG+FO (5 %, w/w) and DG+vitamin E (0·2 %, w/w) groups and were killed after 52 d of treatment. Results indicated that DG significantly decreased the hepatic superoxide dismutase and glutathione peroxidase activities. These alterations were ameliorated both by FO and vitamin E. DG increased the hepatic TAG content approximately by 7·2 % compared with the vehicle control, which was in agreement with the histological alteration. FO, similar to vitamin E, almost normalised the hepatic TAG content and ameliorated the histological characteristics of fatty liver. Similarly, the increased plasma alanine aminotransferase activity induced by DG was normalised by FO and vitamin E, respectively. Faecal bifidobacteria counts were greater in the DG+FO and DG+vitamin E groups compared with the DG group, respectively. In conclusion, the present study indicated that FO diminished the altered hepatic antioxidative enzyme activities and morphology caused by chronic DG administration in Balb/cJ mice, partially associated with its prebiotic role in the colon.