Effect of chronic vanadium administration in drinking water to rats

Abstract

Two-month old Wistar rats of both sexes received, as sole drinking liquid, an aqueous solution of ammonium metavanadate (AMV) at a concentration of 0.01 or 0.05 mg V cm-3 (0.2 or 1.0 mM) for a period of 4 weeks. It was calculated that the animals took up doses of 1.5 and 5-6 mg V kg body weight-1 24 h-1, respectively. Food and AMV solution consumption in the experimental group was similar to food and water consumption in the control group. A statistically significant decrease of consumption of AMV solution at a concentration of 0.05 mg V cm-3 was noted only in males. Hematological examination demonstrated a decrease in the erythrocyte count, hemoglobin level and hematocrit index. This decrease in the erythrocyte count was associated with an increased percentage of reticulocytes in the peripheral blood of the animals drinking the solution with a higher vanadium content. Biochemical analyses demonstrated a decrease of L-ascorbic acid levels in the plasma and erythrocytes of animals drinking the AMV solutions. A distinct tendency for the malonyldialdehyde level to increase in the blood was also observed. Among the enzymes examined in the erythrocytes (catalase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase and delta-aminolevulinic acid dehydratase [ALA-D]) only ALA-D activity was depressed.

Antioxidant enzyme activity and lipid peroxidation in the blood of rats co-treated with vanadium (V+5) and chromium (Cr+3)

“…The unchanged L-ascorbic acid concentration in RBCs between the control and SMV-only treated rats shown in the present experiment (Table 6) was also observed in our previous studies after ammonium metavanadate (AMV) intoxication (Zaporowska et al 1993(Zaporowska et al , 1997. The plasma L-ascorbic acid content did not change either; however, in our earlier studies, its significant decrease in the plasma following vanadate treatment in drinking water was found (Zaporowska et al 1997;Ścibior and Zaporowska 1998;Ścibior 1999).…”

“…However, the results of our study showed that V (as SMV), at the dose of 9 mg V/kg b.w./24 h, ingested by rats in drinking water during 12 weeks, did not have a prooxidant effect on RBCs, which was reflected in the unchanged L-ascorbic acid concentration and MDA level as well as Cu,Zn-SOD, CAT, cGSH-Px, and GR activities in these cells (Tables 6,7,and 8). The unaltered SOD activity in RBCs after treating the rats vanadate in drinking water was also demonstrated in our previous study (Ścibior 1999) and in the studies of Sekar et al (1990), Oster et al (1993) and Russanov et al (1994); whereas the unchanged erythrocyte CAT activity after vanadate intoxication was shown by Sekar et al (1990), Zaporowska et al (1993) and by Russanov et al (1994). The unaltered erythrocyte cGSH-Px activity found in the present experiment was also demonstrated in the studies of Russanov et al (1994) and in our earlier study (Ścibior 1999), but contradictory results showing increased activity (Tas et al 2006) have been reported, too.…”

“…Thus, the above-mentioned effects could take place together, and although the mechanism responsible for the observed increase in the erythrocyte GSH level is not fully clear at present and further studies are necessary to confirm our assumptions, we may claim that the increase probably resulted from an additive and/or an adaptive response to SMV and/or CC exposure. It is important to stress that in our previous studies, in which we observed slightly decreased (Zaporowska et al 1993) or significantly lowered (Ścibior 1999) GSH concentration after vanadate treatment in rats, different experimental conditions were used and this antioxidant was assessed in whole blood, not in RBCs.…”

Opinion of the Scientific Panel on Dietetic products, nutrition and allergies [NDA] related to the Tolerable Upper Intake Level of Vanadium

“…The erythrocyte count was significantly decreased at both dose levels associated with a significant decrease of the haemoglobin level and increased percentage of reticulocytes in the peripheral blood at the highest dose level. In addition, the L-ascorbic acid level in the plasma of males was significantly decreased at both dose levels (Zaporowska et al, 1993).…”

Vanadium in Therapy and Toxicity; Mini-Review and Recommendation of Further Study

“…Several studies have shown that vanadium exposure may cause respiratory dysfunction, 10 hematologic and biochemical alterations, renal toxicity, 11 reproductive and developmental toxicity immunotoxicity, mutagenicity, 12 and neurotoxicity may also occur 13 when readily exposed. In some instances, the cases of death due to exposure to vanadium compounds has also been reported.…”