|South, Paul - FDA, CFSAN, COLLEGE PARK,|
Submitted to: Biological Trace Element Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 9, 2005
Publication Date: January 1, 2006
Citation: South, P.K., Smith, A.D., Guidry, C.A., Levander, O.A. 2006. Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet. Biological Trace Element Research. 109(3):293-300. Interpretive Summary: Early work by other nutritionists has shown that consumption of a diet deficient in both vitamin E and selenium leads to liver damage in rats. Others have also shown that rats fed normal diets but subjected to the stress of physical restraint display evidence of similar liver damage. The purpose of the study presented here was to determine whether restraining mice that had received the doubly deficient diet would result in a greater amount of tissue damage due to an interaction between the feeding of the deficient diet and the stress of immobilization. Our results indicate little evidence for a diet/restraint stress interaction under our conditions. Rather, our results demonstrate the overwhelming impact of the diet in determining the extent of liver damage in this model. This work is important to scientists who study the role of diet functional deficiencies in vitamin E and selenium.
Technical Abstract: Physical restraint has been associated with increased oxidative damage to lipid, protein and DNA. The purpose of this experiment was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin E (VE) deficient diet. Three week-old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden oil was added to the deficient diet to impose an additional oxidative stress. After 4 weeks feeding, half the mice in each group were restrained for 5 days in well-ventilated conical tubes for 8 hours daily. Mice fed the Se and VE deficient diets had increased liver thiobarbituric acid-reactive substance (TBARS)levels and decreased liver glutathione peroxidase (GPX1) activity and a-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained mice fed the adequate diet. Restraint had no effect on liver TBARS or a-tocopherol levels. Liver GPX1 activity, however, was lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase(SOD)activity was lower in the restrained mice fed the adequate or deficient diet. Thus, under our conditions, consumption of the Se and VE deficient diet, but not imposition of physical restraint, significantly increased lipid peroxidation in mice vs. supplemented, unrestrained controls despite the fact that restraint decreased antioxidant protection due to decreased activities of GPX1 and SOD enzymes. Our results demonstrate the importance of dietary intake of antioxidants vs. stress hormones on determining overall in vivo redox status.