| Abstract: | The toxic effect of vanadium (sodium metavanadate) during pregnancy and lactation was studied by feeding vanadium to pregnant,
Sprague-Dawley rats at levels of 1 (control) or 75 μg V/g diet through d 21 postpartum, at which time they were killed. Vanadium-fed
dams had lower food intakes and weight gains than controls during pregnancy. Survival until d 21 postpartum was significantly
lower in the vanadium pups compared to controls. In addition, the surviving pups gained less weight than control pups, despite
similar birth weights. On a relative body weight basis, vanadium pups had larger livers, brains, and testes than controls,
suggesting that these animals were developmentally delayed. Vanadium dams and pups had higher concentrations of hepatic vanadium
than controls. Vanadium pups also had higher concentrations of hepatic zinc than control pups. Maternal hepatic zinc concentrations
were not affected by diet. Also, no significant differences in hepatic iron, copper, or manganese concentrations were observed
for either dams or pups. Hepatic thiobarbituric acid reactivity was higher in whole cell and isolated mitochondria for vanadium
dams and pups than for control dams and pups, indicating that these animals may have had higher levels of lipid peroxidation.
This idea was supported by the observation of lower concentrations of reduced glutathione in the livers of vanadium pups compared
to controls. In contrast, kidney and brain glutathione levels were not affected by diet. In conclusion, animals during periods
of rapid growth are susceptible to vanadium toxicity, and increased lipid peroxidation may be one factor underlying this toxicity. |
