Cytological evaluation of bone marrow smears stained by May-Grünwald Giemsa method was performed. The smears came from 20 fallow deer (Dama dama) 3 days old divided into 2 groups each consisting of 10 animals. The experimental group (E) received intramuscularly selenium and vitamin E at a dose of 3.0 ml (tocopherol acetate – 50 mg, sodium selenite – 0.5 mg, solvent - 1 ml) in the 3rd day of age. The control group (C) did not receive any supplementation or placebo. For hematological analyzes blood was collected three times: on 0, 15th and 25th day of the experiment. Serum concentration of selenium and vitamin E was determined using high perfor- mance liquid chromatography and glutathione peroxidase activity (GSH-Px) by kinetic method. On the 15th day after supplementation, a statistically significant increase in the percentage of erythroblastic cell line was observed in bone marrow smears. At that time, the increase in GSH-Px activity in the E group was also observed, reaching the value of 165.3 U/gHb, which was statisti- cally significant. The percentage of proerythroblasts (8.23% in group E and 5.02% in group C) differed significantly between groups at the 25th day after supplementation. This study revealed that supplementation of selenium and vitamin E resulted in an increase in the number of erythro- cytes to an average of 13.5 (˟ 10¹²/l) in the experimental group on 25th day with a significant increase in hemoglobin to 193 g/l in the experimental group.

The normotensive (Wistar) and spontaneously hypertensive (SHR) rats were examined to assess the response of the organism to selenium (Se) overdose. Moreover, the effect of zinc (Zn) and vitamin E, i.e. dietary components interacting in many biochemical processes with Se, on the Se uptake was evaluated. The control group was fed an untreated diet, and the diets of two other groups were overdosed with Se in the form of sodium selenite (9 mg/kg) and supplemented with Zn (13 mg/kg). Two experimental groups were fed a diet supplemented with Zn (13 mg/kg) and Se at an adequate level (0.009 mg/kg); a half of the animals was supplemented with vitamin

E. The results showed significant differences in the Se contents between the rat strains in case of Se-overdosed groups, where in the liver and kidney tissue Se contents of SHR rats exceeded 3- and 7-fold the normotensive ones. The Se uptake was altered by the vitamin E; no effect of Zn was observed. Activities of antioxidant enzymes were determined in the animal tissues indicating different patterns according to rat strain, tissue analysed, and administered Se dose. Thus, Se overdose, for instance, via an incorrectly prepared dietary supplement, can result in serious imbalances of the biochemical status of the animals.

In this study, we aimed to investigate the effects of vitamin E on mouse adrenal glands in immobilization stress. Twenty-eight male, 10-week-old, BALB/C mice weighing 30-45 grams were divided into four groups. Mice were placed in a cage where no movement was allowed 6 hours/day for 7 days for immobilization stress. 10 ml/kg vitamin E was administered orogastrically 1 hour before immobilization stress in the vitamin E and stress+vitamin E group. At the end of the 7th day, all the animals were subjected to elevated-plus maze (anxiety) and forced swimming (depression) tests. Left adrenal glands were dissected for routine paraffin tissue embedding protocol. Adrenal sections were stained with hematoxylin-eosin and Azan. Malonaldehyde (MDA) levels were also measured in the adrenal tissues. Anxiety level (0.023), depression level (p=0.042) and MDA values (p=0.01) were significantly increased in the stress group. Histological sections of the stress group showed cortical atrophy, medullary hypertrophy, vascular dilation and hemorrhage. Azan staining revealed a thinned capsule and corticomedullary fibrosis in the stress group. Pathologies induced by immobilization stress were mostly reversed after vitamin E administration. The results suggested that vitamin E alleviates adverse effects of immobilization stress (oxidative, behavioral and histopathologic changes) in mice.