Development of nutritional iron deficiency in growing male rats: haematological parameters, iron bioavailability and oxidative defence

• Published in: British journal of nutrition 2011-02, Vol.105 (4), p.517-525
• Main Authors: Alférez, María J. M., Díaz-Castro, Javier, López-Aliaga, Inmaculada, Rodríguez-Ferrer, María, Pérez-Sánchez, Luis Javier, Campos, Margarita S.
• Format: Article
• Language: English
• Subjects: Animal Nutrition Sciences; Animals; Antioxidants; Bioavailability; Biological and medical sciences; Catalase - metabolism; Cytosol - metabolism; Diet; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Glutathione Peroxidase - metabolism; Hematology; Hematology - methods; Iron; Iron - deficiency; Iron - metabolism; Iron - pharmacology; Male; Males; Metabolism; Metabolism and Metabolic Studies; Nutrient deficiency; Oxidative Stress; Physical growth; Rats; Rats, Wistar; Rodents; Superoxide Dismutase - metabolism; Thiobarbituric Acid Reactive Substances - metabolism; Time Factors; Transferrin - metabolism; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Vitamin deficiency
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1017/S0007114510004046

Despite Fe deficiency having been widely studied, the sequence of events in its development still remains unclear. The aim of the present study was to elucidate the effects of nutritional Fe-deficiency development on haematological parameters, Fe bioavailability and the enzymes involved in oxidative defence in recently weaned male Wistar albino rats. Control (C) and Fe-deficient (ID) groups were fed the AIN-93 G diet with a normal Fe level (45 mg/kg diet) or with a low Fe level (5 mg/kg diet), respectively, for 20, 30 or 40 d. At day 20 serum Fe, serum ferritin and the saturation of transferrin decreased drastically, decreasing further in the course of Fe-deficiency development for the saturation of transferrin. The development of Fe deficiency did not affect plasma thiobarbituric acid-reactive substance production, or catalase (CAT) and glutathione peroxidase (GPx) activities in erythrocyte cytosol. Fe deficiency diminished hepatic Fe content and CAT and GPx activities in hepatic cytosol only at day the 20. However, in spite of the minor Fe deposits in the brain of ID rats, the CAT and GPx activities in the brain cytosolic fraction did not differ in any of the studied periods v. control rats. These results show that brain is a tissue that does not seem to depend on Fe levels for the maintenance of antioxidant defence mechanisms in the course of nutritional Fe deficiency.