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Dietary ascorbic acid and selenium relationships in the guinea pig.
Annals of Nutrition & Metabolism
|January 1, 1987
Summary
Dietary ascorbic acid (AA) does not affect selenium (Se) levels in guinea pigs. However, higher AA intake significantly boosts Se-dependent glutathione peroxidase (GPx) activity in plasma, liver, and erythrocytes.
Area of Science:
- Biochemistry
- Nutritional Science
- Toxicology
Background:
- Selenium (Se) is an essential trace element crucial for antioxidant defense, primarily through Se-dependent glutathione peroxidase (GPx) enzymes.
- Ascorbic acid (AA), or vitamin C, is a potent antioxidant that may interact with Se metabolism and GPx activity.
- Understanding the interplay between dietary AA and Se is vital for optimizing antioxidant status and health outcomes.
Purpose of the Study:
- To investigate the impact of varying dietary levels of ascorbic acid (AA) and selenium (Se) on Se-dependent glutathione peroxidase (GPx) activity and tissue Se levels in guinea pigs.
- To determine if dietary AA influences Se bioavailability or Se-dependent enzyme activity.
Main Methods:
- Guinea pigs were fed a semipurified diet with different concentrations of AA (0, 200, 400 mg/kg) and Se (0.05, 0.2 ppm) for 24 days.
- Plasma, erythrocyte, and liver concentrations of AA and Se were measured.
- Se-dependent GPx activity was assessed in plasma, erythrocytes, and liver tissue.
Main Results:
- Plasma, erythrocyte, and liver AA concentrations increased proportionally with dietary AA intake.
- Higher dietary Se significantly increased erythrocyte and liver Se levels, independent of AA.
- Dietary AA significantly increased plasma, erythrocyte, and liver GPx specific activities, irrespective of Se levels.
Conclusions:
- Dietary ascorbic acid (AA) does not alter tissue selenium (Se) levels in guinea pigs.
- Ascorbic acid (AA) significantly enhances the activity of Se-dependent glutathione peroxidase (GPx) in plasma, erythrocytes, and liver.
- These findings highlight a synergistic role of AA in supporting antioxidant defense mechanisms mediated by GPx, independent of Se tissue accumulation.