Functional and morphological olfactory bulb modifications in mice after vanadium inhalation.

Neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases, have olfaction impairment. These pathologies have also been linked to environmental pollutants. Vanadium is a pollutant, and its toxic mechanisms are related to the production of oxidative stress. In this study, we evaluated the effects of inhaled vanadium on olfaction, the olfactory bulb antioxidant, through histological and ultrastructural changes in granule cells. Mice in control group were made to inhale saline; the experimental group inhaled 0.02-M vanadium pentoxide (V2O5) for 1 hr twice a week for 4 weeks. Animals were sacrificed at 1, 2, 3, and 4 weeks after inhalation. Olfactory function was evaluated by the odorant test. The activity of glutathione peroxidase (GPx) and glutathione reductase (GR) was assayed in olfactory bulbs and processed for rapid Golgi method and ultrastructural analysis. Results show that olfactory function decreased at 4-week vanadium exposure; granule cells showed a decrease in dendritic spine density and increased lipofuscin, Golgi apparatus vacuolation, apoptosis, and necrosis. The activity of GPx and GR in the olfactory bulb was increased compared to that of the controls. Our results demonstrate that vanadium inhalation disturbs olfaction, histology, and the ultrastructure of the granule cells that might be associated with oxidative stress, a risk factor in neurodegenerative diseases.