Oral administration of ammonium metavanadate and potassium dichromate distorts the inflammatory reaction induced by turpentine oil injection in male rats

Abstract

Heavy metal pollution is rapidly increasing in the environment. It has been shown that exposure to vanadium and chromium is able to alter the immune response. Nevertheless, the mechanisms by which these metal pollutants mediate their immunomodulatory effects are not completely understood. Herein, we examined the effect of ammonium metavanadate and potassium dichromate on the development of an inflammatory response caused by subcutaneous injection of turpentine oil. We demonstrated that pretreatment of rats with ammonium metavanadate and potassium dichromate for two weeks prior to initiation of the inflammatory response resulted in a wider zone of necrosis surrounding the site of inflammation. The acute inflammatory process in the combined model was characterized by elevated serum levels of IL-10 and decreased serum levels of IL-6 as compared to rats not treated with ammonium metavanadate and potassium dichromate. Ammonium metavanadate and potassium dichromate administration induced a decrease in the proportion of splenic His48^HighCD11b/c⁺ myeloid cells accompanied by a reduced infiltration of the wound with neutrophils. Further analysis showed decreased proportions of CD3⁺CD4⁺IFNγ⁺ and CD3⁺CD4⁺IL-4⁺ T cells in the rats with combined model as compared to inflamed rats not treated with ammonium metavanadate and potassium dichromate. The data suggest that consumption of vanadium and chromium compounds disrupts the inflammatory response through an altered balance of pro- and anti-inflammatory cytokines and inhibition of effector T cell activation and neutrophil expansion.

Keywords:

• Ammonium metavanadate
• potassium dichromate
• aseptic inflammation
• myeloid cells
• T cells

Acknowledgments

The authors thank Theodore Micceri, Ph.D. for critical reading of the manuscript.

Disclosure statement

The authors declare that they have no competing interests.

Additional information

Funding

This study was supported by the Science Committee of Ministry of Education and Science of the Republic of Kazakhstan under Grant #3164GF4 “Biomolecular features of ecology and immunodeficiency associated aseptic inflammation process”, #AP05131710 “Pharmacological approaches to target myeloid-derived suppressor cells (MDSCs) for suppression of chronic inflammation as a stimulant of tumor growth in experimental models” and Grant #AP05131691 “Molecular mechanisms of influence of T regulatory cells on tumor cell activity”.