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Evaluation of Immunotoxicity of Sodium Metavanadate Following Drinking Water Exposure in Female B6C3F1/N Mice in a 28-day Study

Rachel Frawley, Victor J. Johnson, Gary R. Burleson, Keith R Shockley, Mark F. Cesta, Greg Travlos, Michelle Cora, Georgia Roberts, Dori Germolec

TOX-106 Vanadium Compounds (Sodium Metavanadate and Vanadyl Sulfate): Abstract for TOX-106
DOI: https://doi.org/10.22427/NTP-DATA-500-001-001-000-7



Sodium metavanadate (NaVO₃) is a pentavalent vanadium compound used in the metal industry and in dietary supplements; human exposure occurs through inhalation of fumes and dust, and ingestion of NaVO₃-containing products. The objective of this study was to assess the potential immunotoxicity of NaVO₃. Female B6C3F1/N mice were exposed to 0-500 ppm NaVO₃ in drinking water for 28 days and evaluated for effects on immune cell populations, and innate, cellular-, and humoral-mediated immunity. There was a decreasing trend in body weight (BW) and BW gain in NaVO₃ exposed mice, with a significant (p≤0.05) decrease in BW gain at ≥ 250 ppm, relative to control. Conversely, increasing trends in spleen weights, and an increase (p≤0.05) in the spleen:BW ratio at ≥250 ppm NaVO₃ were observed. NaVO₃ exposure altered antibody production against sheep red blood cells (SRBC). Antibody forming cells (AFC)/10⁶ spleen cells exhibited a decreasing trend, with a significant decrease (p≤0.05) at 500 ppm NaVO₃, concurrent with an increase in percent B-cells. NaVO₃ had no effect on the serum anti-SRBC IgM antibody titers or antibody production against keyhole limpet hemocyanin. Exposure to NaVO₃ decreased the percentage of natural killer (NK) cells at all dose levels (p≤ 0.05), however, the lytic activity of NK cells was not affected. NaVO₃ altered T-cell populations at 500 ppm but had no effect on T-cell proliferative responses or the lytic activity of cytotoxic T-cells. Collectively, these data indicate that NaVO₃ induced alterations in humoral-mediated immunity, specifically the AFC response, with no effect on cell-mediated or innate immunity.

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