Alpha-tocopherol concentrations, lipid peroxidation and superoxide dismutase and glutathione peroxidase activities in rat heart and liver after feeding stabilized and unstabilized fish oil
2001
Luostarinen, R.L. | Laasonen, K. | Calder, P.C.
To further examine the relationship between increased consumption of n-3 polyunsaturated fatty acids (PUFAs), antioxidant defence systems and lipid peroxidation, for 6 weeks adult male rats were fed fish oil (FO)-rich diets containing one of two levels of alpha-tocopherol (4.5 or 1.9 IU vitamin E/g fish oil) either with or without the addition of the antioxidant mix PUFANOX in order to stabilize the FO; rats fed corn oil or butter served as controls. Feeding FO resulted in increased proportions of the n-3 PUFAs eicosapentaenoic and docosahexaenoic acids in the phospholipids of the plasma, myocardium and liver. Rats fed the PUFANOX-stabilized FO had higher plasma, myocardial and liver alpha-tocopherol concentrations compared to those fed the unstabilized FO; alpha-tocopherol concentrations were highest in rats fed the higher level of alpha-tocopherol in combination with PUFANOX. FO feeding increased lipid peroxidation in myocardial and liver extracts. This was highest after feeding the FO diet which contained the lower amount of alpha-tocopherol and no PUFANOX and was positively correlated with the n-3 PUFA content of the phospholipids. FO feeding did not alter myocardial and liver superoxide dismutase activity. Myocardial glutathione peroxidase activity was lower after feeding FO, except that containing the higher amount of alpha-tocopherol plus PUFANOX. Glutathione peroxidase activity in the liver was lower after FO feeding than after corn oil with no significant differences among the different FO diets. Thus, insufficient antioxidant protection in FO results in decreased antioxidant defences and increased lipid peroxidation. Increasing the content of alpha-tocopherol and including a stabilizing agent (e.g. PUFANOX) in FO can prevent at least some of these effects. The results of the present study do not support the idea that intake of FO, by increasing tissue lipid peroxidation, induces the body's antioxidant defence system.
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