| Abstract: | Adult male CD-1 mice were treated with various levels of vanadate in drinking water for 30 days. The levels of catecholamine and indoleamine neurotransmitters and their major metabolites were measured in six different brain regions. Vanadium caused a dose-related decrease in norepinephrine (NE) levels in hypothalamus, the region rich in this biogenic amine. Levels of the NE metabolite, vanillylmandelic acid (VMA), correspondingly decreased in the same region. Although hypothalamic dopamine (DA) also showed a significant decline, vanadium had little effect on DA metabolites. Levels of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were not influenced. Levels of DA were not affected in the corpus striatum, where the highest levels of this amine are observed. Effects of vanadium on various biogenic amines and their metabolites were only marginal in other brain regions. Results suggest that vanadium has a selective effect on adrenergic pathways, and effects on other hypothalamic amines appear to be secondary. These observations support the pro-oxidant potential of vanadate ion on catecholamines suggested earlier. |
