Objective To observe the effects of subchronic sodium metavanadate exposure on brain development and cell apoptosis in hippocampus, cortex, and striatum of rats.
Methods Healthy male SD rats (n=49) weaned at 21 d of age were randomly divided into one blank control and three vanadium groups 0.5, 1.0, and 2.0 mg/mL sodium metavanadate (NaVO3). After administration via drinking water for 3 months, necroscopy was conducted to determine the weight coefficient of brain and observe the histological changes in hippocampus, cortex, and striatum. Cell apoptosis in hippocampus, cortex, and striatum was detected by flow cytometry.
Results The organ coefficients of brain for the 0.5 mg/mL vanadium group (0.466& #177;0.077), 1.0 mg/mL vanadium group (0.470& #177;0.058), and 2.0 mg/mL vanadium group (0.712& #177;0.262) were higher than that in the control group (0.392& #177; 0.023) (P<0.05), and the 2.0 mg/mL vanadium group presented higher values than the 0.5 mg/mL and 1.0 mg/mL vanadium groups (P<0.05). HE staining showed tissue loose, edema, and capillary expansion in the hippocampus, cortex, and striatum of vanadium treated groups, as well as scattered eosinophilic changes, neuron apoptosis, and neuronophagia. In hippocampus, the early apoptosis rates and the total apoptosis rates for the 1.0 mg/mL vanadium group (7.45%, 7.55%) and 2.0 mg/mL vanadium group (14.30%, 15.00%) were higher than those of the control group (1.65%, 1.75%), and the 2.0 mg/mL vanadium group also presented higher values than the 0.5 mg/mL vanadium group (4.10%, 4.10%) (P<0.01). In striatum, the early apoptosis rates and the total apoptosis rates for the 1.0 mg/mL vanadium group (9.50%, 9.80%) and 2.0 mg/mL vanadium group (13.55%, 14.65%) were higher than those of the control group (2.15%, 2.35%) (P<0.01). In cortex, the early apoptosis rates and the total apoptosis rates for the 1.0 mg/mL vanadium group (10.65%, 11.10%) and 2.0 mg/mL vanadium group (16.75%, 17.40%) were higher than those of the control group (3.15%, 3.15%), those of the 2.0 mg/mL vanadium group were higher than those of the 1.0 mg/mL vanadium group (8.30%, 8.55%) (P<0.01), and late apoptosis showed similar patterns that the 1.0 mg/mL (0.45%) and 2.0 mg/mL (0.50%) groups reported higher rates than the control group (P<0.01).
Conclusion Subchronic exposure to vanadium leads to cell apoptosis in hippocampus, cortex, and striatum of rats, affecting the development of brain.
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