Oral administration of ammonium metavanadate and potassium dichromate distorts the inflammatory reaction induced by turpentine oil injection in male rats
Balabekova M.K. Ostapchuk Y.O. Perfilyeva Y.V. Tokusheva A.N. Nurmuhambetov A. Tuhvatshin R.R. Trubachev V.V. Akhmetov Z.B. Abdolla N. Kairanbayeva G.K. Sulev K. Belyaev N.N.
2021Taylor and Francis Ltd.
Drug and Chemical Toxicology
2021#44Issue 3277 - 285 pp.
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 His48HighCD11b/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.
Ammonium metavanadate , aseptic inflammation , myeloid cells , potassium dichromate , T cells
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Department of Pathological Physiology, S.D. Asfendiyarov Kazakh National Medical University, Almaty, Kazakhstan
Laboratory of Molecular Immunology and Immunobiotechnology, M.A. Aitkhozhin’s Institute of Molecular Biology and Biochemistry, Almaty, Kazakhstan
Department of Pathophysiology, I.K. Akhunbaev Kyrgyz State Medical Academy, Bishkek, Kyrgyzstan
Department of Pathophysiology, University of Tartu, Tartu, Estonia
Department of New Technology, Saint-Petersburg Pasteur Institute, Saint-Petersburg, Russian Federation
Department of Pathological Physiology
Laboratory of Molecular Immunology and Immunobiotechnology
Department of Pathophysiology
Department of Pathophysiology
Department of New Technology
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