The role of V as a micronutrient, and its hypoglycaemic and toxicological activity, have yet to be completely established. The present study focuses on changes in the bioavailability and tissue distribution of Se in diabetic streptozotocin rats following treatment with V. The following four study groups were examined: control; diabetic (DM); diabetic treated with 1 mg V/d (DMV); diabetic treated with 3 mg V/d (DMVH). V was supplied in the drinking water as bis(maltolato)oxovanadium (IV). The experiment had a duration of 5 weeks. Se was measured in food, faeces, urine, serum, muscle, kidney, liver and spleen. Glucose and insulin serum were studied, together with glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione transferase (GST) activity and malondialdehyde (MDA) levels in the liver. In the DM group, we recorded higher levels of food intake, Se absorbed, Se retained, Se content in the kidney, liver and spleen, GSH-Px and GST activity, in comparison with the control rats. In the DMV group, there was a significant decrease in food intake, Se absorbed, Se retained and Se content in the liver and spleen, and in GSH-Px and GST activity, while fasting glycaemia and MDA remained unchanged, in comparison with the DM group. In the DMVH group, there was a significant decrease in food intake, glycaemia, Se absorbed, Se retained, Se content in the kidney, liver and spleen, and in GSH-Px and GST activity, and increased MDA, in comparison with the DM and DMV groups. We conclude that under the experimental conditions described, the treatment with 3 mg V/d caused a tissue depletion of Se that compromised Se nutritional status and antioxidant defences in the tissues.

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.

Numerous mechanisms have been proposed to explain the anti-carcinogenic effects of Se, among them altered carcinogen metabolism. We investigated the effect of Se supplementation on activities of glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione S-transferase (GST) in different blood compartments, and expression of selected phase 1 and phase 2 genes in leucocytes (GPX1, γ-glutamylcysteine ligase catalytic subunit (GCLC), AP-1 transcription factor Fos-related antigen 1 (Fra1), NAD(P)H:quinone oxidoreductase (NQO1), and aryl hydrocarbon receptor repressor (AhRR)). Healthy elderly Danes (n 105; age 71·3 (sd 4·26) years; 36 % reporting use of multivitamin/mineral supplements) participated and were supplemented daily for 5 years with placebo, 100 μg, 200 μg or 300 μg Se as Se-enriched yeast (SelenoPrecise®). Blood samples were collected after 5 years of intervention. When all four groups were compared we found no effect of Se supplementation on plasma GPX or GR, on erythrocyte GPX, GR or GST, or on thrombocyte GR or GST. We found increased thrombocyte GPX activity at the two highest dosage levels in women only, but not in men. No effects on GPX1, NQO1 or AhRR gene expression were found. When all Se-supplemented groups were pooled we found significant down regulation of the expression of some phase 2 genes (GCLC, Fra1). A significant increase in AhRR gene expression with smoking was found but was independent of Se supplementation. Down regulation of phase 2 genes could increase the risk of cancer. However, further studies are needed to establish whether the observed effect in leucocytes reflects a similar expression pattern in target tissues.

Increased Se intakes have been associated with decreased risk of cancer and CVD. Several mechanisms have been proposed, including antioxidant effects through selenoproteins, induction of carcinogen metabolism and effects on the blood lipid profile. In a 4 × 1 week randomised, double-blind cross-over study, healthy young men supplemented their usual diet with selenate, Se-enriched yeast, Se-enriched milk or placebo (Se dose was 300 μg/d for selenate and Se-enriched yeast, and about 480 μg/d for Se-enriched milk) followed by 8-week washout periods. All Se sources increased serum Se levels after supplementation for 1 week. The effect of the organic forms did not differ significantly and both increased serum Se more than selenate. Conversely, thrombocyte glutathione peroxidase (GPX) was increased in the periods where subjects were supplemented with selenate but not in those where they were given Se-enriched yeast or Se-enriched milk. We found no effect on plasma lipid resistance to oxidation, total cholesterol, TAG, HDL- and LDL-cholesterol, GPX, glutathione reductase (GR) and glutathione S-transferase (GST) activities measured in erythrocytes, GPX and GR activities determined in plasma, or GR and GST activities in thrombocytes. Leucocyte expression of genes encoding selenoproteins (GPX1, TrR1 and SelP), and of electrophile response element-regulated genes (GCLC, Fra1 and NQO1) were likewise unaffected at all time points following intervention. We conclude that thrombocyte GPX is specifically increased by short-term selenate supplementation, but not by short-term supplementation with organic Se. Short-term Se supplementation does not seem to affect blood lipid markers or expression and activity of selected enzymes and a transcription factor involved in glutathione-mediated detoxification and antioxidation.