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

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.

Trace elements and ALAD gene polymorphisms in general population from three uranium legacy sites - A case study in Kyrgyzstan.

At three uranium (U) legacy sites in Kyrgyzstan, namely, Kadji Sai, Mailuu-Suu and Sumsar, an initial human bio-monitoring programme was introduced as a complementary activity to environmental impact studies in these areas. The aim was to assess trace element (TE) contents in blood and genetic susceptibility for Pb as one of the contaminants. The programme included the determination of 9 TE in blood samples from 123 residents living permanently in this environment. The analyses included U and the potentially toxic TE, lead (Pb), cadmium, mercury (Hg), and arsenic (As), together with essential elements iron (Fe), copper, selenium (Se) and manganese (Mn). TE were analysed by inductively coupled plasma mass spectrometry (ICPMS) and genetic background effect by three single nucleotide polymorphisms (SNPs) of delta-aminolevulinic acid dehydratase (ALAD; rs1805313, rs818708, rs1800435) genotyped by quantitative polymerase chain reaction (qPCR). The obtained results were generally similar to literature reference values obtained from the U non-exposed environments. However, some significant findings indicated elevated levels of certain contaminants typical of the studied environment (U, Pb). Several essential (Se, Mn) and toxic TE (Pb, Hg, As, U) in blood showed statistically significant differences among the studied areas. All areas showed diminished Fe blood levels. Altogether, this indicated specific and different environmental conditions at three industrial legacy sites for U milling and processing along with the accompanying chemical (pollutant) elements. Blood U concentrations were slightly higher at Mailuu-Suu, known for elevated technogenic and naturally occurring U. At Sumsar, the distribution of elevated blood Pb concentrations indicated an airborne source of pollution that was different from the anticipated aqueous exposure pathway. Pb blood variability was found associated with ALAD polymorphisms (SNPs rs1805313, rs1800435). Results are confirming that human data will be a useful and scientifically important additional tool for environmental impact assessment studies at industrial legacy sites in Kyrgyzstan.