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Published on: February 7, 2018
Oxidative stress and antioxidant status in mouse kidney: effects of dietary lipid and vitamin E plus iron
1Department ofNutrition and Food Science, University of Kentucky, Lexington, KY 40506-0054, USA.
Abstract:
The purpose of this study was to determine the effects of dietary fat, vitamin E, and iron on oxidative damage and antioxidant status in kidneys of mice. Sixty 1-month-old male Swiss-Webster mice were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g all-rac-alpha-tocopherol acetate or 0.74 g ferric citrate per kilogram of diet for 4 weeks. Significantly (P < 0.05) higher levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), and conjugated dienes were found in the kidneys of mice fed with fish oil compared with mice fed lard irrespective of vitamin E status. Mice maintained on a vitamin E-deficient diet had significantly higher renal levels of TBAR, but not conjugated dienes, than the supplemented group. Fish oil fed mice receiving vitamin E supplementation had lower levels of alpha-tocopherol than did mice in the lard fed group. Significantly higher levels of ascorbic acid were also found in the kidneys of mice fed with fish oil than were found in mice fed lard. The levels of protein carbonyls and glutathione (GSH), and activities of catalase, superoxide dismutase, selenium (Se)-GSH peroxidase, and non-Se-GSH peroxidase were not significantly altered by dietary fat or vitamin E. Dietary iron had no significant effect on any of the oxidative stress and antioxidant indices measured. The results obtained provide experimental evidence for the pro-oxidant effect of high fish oil intake in mouse kidney and suggest that dietary lipids play a key role in determining cellular susceptibility to oxidative stress.
Insights
High fish oil intake increases kidney oxidative damage in mice, while vitamin E offers some protection. Dietary iron had no significant impact on these oxidative stress markers.
Area of Science:
- * Nutritional biochemistry and toxicology
- * Renal oxidative stress and antioxidant defense mechanisms
Background:
- * Dietary lipids, particularly polyunsaturated fatty acids, can influence oxidative stress.
- * Vitamin E (alpha-tocopherol) is a key lipid-soluble antioxidant crucial for protecting cell membranes.
- * Iron is essential for cellular metabolism but can also catalyze oxidative reactions.
Purpose of the Study:
- * To investigate the impact of dietary fat (fish oil vs. lard) and vitamin E supplementation on kidney oxidative damage.
- * To assess the role of dietary iron in modulating oxidative stress and antioxidant status in mouse kidneys.
- * To determine how these dietary factors affect specific biomarkers of lipid peroxidation and antioxidant capacity.
Main Methods:
- * Sixty male Swiss-Webster mice were fed a basal vitamin E-deficient diet for 4 weeks.
- * Diets varied in fat source (fish oil/corn oil vs. lard) and included vitamin E (all-rac-alpha-tocopherol acetate) and iron (ferric citrate) supplementation.
- * Kidney tissues were analyzed for lipid peroxidation products (TBAR, conjugated dienes), protein carbonyls, and antioxidant levels (ascorbic acid, glutathione, enzyme activities).
Main Results:
- * Fish oil-rich diets significantly increased kidney lipid peroxidation products (TBAR, conjugated dienes) compared to lard diets, regardless of vitamin E status.
- * Vitamin E deficiency led to higher renal TBAR levels, indicating increased oxidative damage.
- * Fish oil-fed mice showed lower vitamin E levels and higher ascorbic acid levels in kidneys; dietary iron had no significant effect on measured oxidative stress or antioxidant indices.
Conclusions:
- * High dietary fish oil intake exerts a pro-oxidant effect on mouse kidneys.
- * Dietary lipids play a critical role in determining cellular susceptibility to oxidative stress.
- * Vitamin E supplementation can mitigate some of the oxidative damage induced by fish oil, though iron's role was not significant in this study.