Toxic effects of long-term intratracheal administration of vanadium pentoxide in rats.

The toxic effects of vanadium pentoxide were investigated following chronic exposure. Rats were exposed intratracheally once a month (0.56 mg V2O5/kg) for 12 months. Body weight gain of exposed animals slowed down following the 10th treatment when compared to the corresponding controls. Lung weights were significantly greater than controls; however, other organ weights were not changed. Blood glucose of treated animals was slightly decreased whereas blood total cholesterol was reduced markedly. The in vitro experiments were performed to explain the mechanism of chronic toxic effects. The results of these experiments confirmed that vanadium(V) undergoes one-electron redox cycling in rat lung biomembranes and that reoxidation of vanadium(IV) initiates lipid peroxidation under aerobic conditions. The lung is the primary target organ during the intratracheal exposure to V2O5. It is postulated that free-radical redox cycling of vanadium may be responsible for the observed pulmonary toxicity.