Selenium is an essential trace element for mammals. Through selenoproteins, this mineral participates in various biological processes such as antioxidant defence, thyroid hormone production, and immune responses. Some reports indicate that a human organism deficient in selenium may be prone to certain diseases. Adverse health effects following selenium overexposure, although very rare, have been found in animals and people. Contrary to selenium, arsenic and cadmium are regarded as toxic elements. Both are environmental and industrial pollutants, and exposure to excessive amounts of arsenic or cadmium can pose a threat to many people's health, especially those living in polluted regions. Two other elements, vanadium and chromium(III) in trace amounts are believed to play essential physiological functions in mammals. This review summarizes recent studies on selenium interactions with arsenic and cadmium and selenium interactions with vanadium and chromium in mammals. Human studies have demonstrated that selenium may reduce arsenic accumulation in the organism and protect against arsenic-related skin lesions. Selenium was found to antagonise the prooxidant and genotoxic effects of arsenic in rodents and cell cultures. Also, studies on selenium effects against oxidative stress induced by cadmium in various animal tissues produced promising results. Reports suggest that selenium protection against toxicity of arsenic and cadmium is mediated via sequestration of these elements into biologically inert conjugates. Selenium-dependent antioxidant enzymes probably play a secondary role in arsenic and cadmium detoxification. So far, few studies have evaluated selenium effects on chromium(III) and vanadium actions in mammals. Still, they show that selenium may interact with these minerals. Taken together, the recent findings regarding selenium interaction with other elements extend our understanding of selenium biological functions and highlight selenium as a potential countermeasure against toxicity induced by arsenic and cadmium.

The purpose of these studies was to evaluate the effect of selected vanadium and magnesium doses on certain haematological and biochemical blood parameters in rats. Outbred 2-month-old, albino male Wistar rats received for a period of 6 weeks, as a sole drinking liquid, the following water solutions: group II, sodium metavanadate (SMV) at a concentration of 0.125 mg V/mL; group III, magnesium sulphate (MS) at a concentration of 0.06 mg Mg/mL; and group IV, SMV-MS solution at the same concentrations. The control group received at this time deionized water to drink. It was calculated that group II ingested with drinking water about 10.7 mg V/kg b. w./24 h, group III 6 mg Mg/kg b. w./24 h, and group IV about 9 mg V and 4.5 mg Mg/kg b. w./24 h. The exposure to vanadium alone (group II) led to a statistically significant decrease in body weight gain, food and fluid intakes. Moreover, in the same group of rats a statistically significant decrease in the RBC count, Hb concentration, MCV, and MCH values was demonstrated. Additionally, a statistically significant decrease in the plasma L-ascorbic acid concentration and a significant increase in MDA concentration in blood in this group were found. Instead, after the administration of magnesium alone (group III), a statistically significant decrease in the fluid intake and in the L-ascorbic acid concentration in plasma was noted. Furthermore, in the same group of rats a statistically significant increase in Hb level and in the plasma magnesium concentration was demonstrated. Two-way analysis of variance (ANOVA) did not reveal the interactions between V and Mg.

The effect of V(5+) and Mg treatment on spontaneous and stimulated lipid peroxidation (LPO) was studied in liver supernatants obtained from outbred 5-month-old, albino male Wistar rats. The 2-month-old animals daily received deionized water to drink (control, group I); group II - water solution of NaVO(3) (SMV) at a concentration of 0.125 mg V ml(-1); group III - water solution of MgSO(4) (MS) at a concentration of 0.06 mg Mg ml(-1), group IV - water solution of SMV-MS at the same concentrations as in groups II and III for V and Mg, respectively, over a 12-week period. Three metal salts were selected as agents that may modify the LPO process (FeSO(4), NaVO(3) and MgSO(4)). V-intoxicated rats and those treated with V and Mg in combination had higher liver spontaneous malondialdehyde (MDA) formation, compared with the control and Mg-supplemented animals. In the same groups of animals the total antioxidant status (TAS) was also significantly lowered, in comparison with the control. In the supernatants obtained from the above-mentioned groups of rats a significant increase in MDA concentration was found in the presence of exogenous 30 microm FeSO(4) as well as 30, 100, 200 and 400 microm NaVO(3), compared with groups I and III. Significantly elevated MDA production was also observed in the supernatants obtained from the rats exposed to V and Mg in combination in the presence of exogenous 100 and 200 microm MgSO(4) in comparison with the control and group III as well as in the presence of exogenous 400 and 600 microm MgSO(4) compared only with group III. In vitro treatment with 1000 microm MgSO(4 )of control liver supernatants and those obtained from group III significantly enhanced MDA level, compared with spontaneous MDA formation. The two-way ANOVA indicated that the changes in the basal MDA level and in TAS in the rats at combined V and Mg application, were not due to V-Mg interaction, but resulted from independent action of V. In addition, the three-way ANOVA revealed that the changes in LPO induced by in vitro treatment of liver supernatants with exogenous Fe or V or Mg (600, 800 and 1000 microm) were a consequence of independent action of those metals and they also resulted from the interactions between Fe(exog) and V(end) and between V(end) and V(exog). In conclusion, V consumed by the rats with drinking water at a dose of 12 mg V kg(-1) body weight per 24 h for 12 weeks decreased TAS and enhanced spontaneous LPO in the hepatic tissue, which confirms its pro-oxidant potential, was also found in in vitro conditions with regard to LPO. Mg administered to rats in combination with V, at the concentration used, neither reduced nor intensified the basal LPO, compared with V-only treated animals; however, its stimulating effect on LPO was revealed in in vitro conditions, which requires further study.