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Mercury is present in nature as metallic mercury, inorganic and organic compounds. Mercury levels constantly increase in the human natural environment. A similar rise of mercury content has been observed in human tissues. Kidney disease arising from exposure to heavy metals, mainly during occupational exposure to mercury, may play a special role in nephrology. Long-term exposure to mercury may cause progressive degenerative changes in the kidneys, possibly leading to renal insufficiency. The main renal changes caused by mercury are indicated by the both glomerular and tubular disfunction. Early renal damage may usually be monitored by measurements in urine excretion of very sensitive small proteins and of some enzymes. This article reviews data concerning the nephrotoxic effects of mercury compounds in animals and humans induced by exposure to mercury compounds with the results of our study in changes of proteins in urine excretion in groups of workers occupationally exposed to mercury vapours, (depending on degree and duration of exposure).
The immunological effects of the environmental and/or occupational exposure to NO2 and NO in air as polluting gases have been examined in groups of 16 men. The determina-tion of NO2 and NO concentrations in ambient air in the work enviroment as well as in ambient air in residential areas of these men was performed, always by use of an Amaya-Sugiura passive sampling spectrophotometric method. Mean concentration of NO2 in ambient air in residential areas was 0.0210 mg x m-3 (0.0070 to 0.0470). NO2and NO mean concentrations in ambient air in the work enviroment were 0.0867 mg x m-3 (0.0165 to 0.1960) and 0.0614 mg x m-3 (0.0220 to 0.1090) respectively. For the determination of T-cell and (CD19+)B-cells populations Behring monoclonal antibodies were used in indirect immuno-fluores-cence tests. The serum levels of immunoglobulins: G, A, M, E; C3c and C4 complement components; total circulating immunological complexes (CIC) as well as acute phase proteins: C-reactive protein (CRP), haptoglobin, ceruloplasmin and transferrin were determined by nephelometry. Stimulation T-cell line in exposed to NO2 and NO was evidenced by in-creased number of (CD3+)T-cells, by about twice (p<0.001) increased number of (CD4+)T-helper cells and by increased number of (CD8+)T-suppressor cells. The higher increase in count of (CD4+)T-helper cells than (CD8+)T-suppressor cells population caused the increased value of the (CD+4)T-helper/(CD8+)T-suppressor ratio by about 25% (p<0.01) in the men exposed to NO2 and NO. No changes were observed in the number of (CD19+)B-cells as well as in the (CD3+)T/(CD8+)T-suppressor ratio. In men of exposed to NO2 and NO elevation of IgG serum concentration by a 17.7% (p<0.01) was evidenced as well as decreased of C3c by 18.6% (p<0.001) and C4 by 35% (p<0.001), whereas total CIC in serum was elevated by about twice (p<0.001). Significant positive correlations between concentrations of NO2 in air and numbers of total lymphocytes, (CD3+)-cells, (CD4+)T-helper, (CD8+)T-suppressor cells or IgG (/r/ from 0.31 to 0.71) as well as significant negative correlations between concentrations in air of NO2 and IgE, C3c, CRP or haptoglobin (/r/ from -0.49 to -0.31) were calculated. Moreover, significant positive correlation between NO concentrations in air in work place and counts of (CD3+)T-, (CD8+)T-suppressor, (CD19+)B-cells and levels in serum of C4, haptoglobin and ceruloplasmin (/r/ from 0.33 to 0.63) as well as significant negative correlations between NO concentrations in air in work place and serum levels of IgG, IgA and IgM (/r/ from -0.67 to -0.47) were also observed. In conclusion, environmental exposure to NO2 and NO can modificate in the peripheral blood of humans the parameters of cell-mediated and/or humoral immunity.
The immunological effects of environmental and/or occupational exposure to S02 in air as polluting gas have been examined in a group of 21 exposed men. The determination of S02 concentrations in ambient air in the work enviroment as well as in ambient air in residential areas of these men was performed, always using Amaya-Sugiura passive sampling and ion spectrophotometry. Mean concentration of S02 in ambient air in residential areas was 0.5792 mg • m-3 ± 0.2871 (0.22 to 1.52). Mean concentration of S02 in ambient air in the work enviroment was 2.2612 ± 2.1477 mg • m-3 (0.47 to 9.57). For the determination of T-cells and (CD19+)B-cell populations Behring monoclonal antibodies were used in indirect immunofluorescence tests. The serum levels of immunoglobulins: G, A, M, E; C3c and C4 complement components; total circulating immune complexes (CIC) as well as acute phase proteins: C-reactive protein (CRP), haptoglobin, ceruloplasmin and transferrin were determined by nephelometry. The mean number of total lymphocytes in men exposed to S02 was increased by 43% (p < 0.001). The stimulation T-cell line exposed to S02 was evidenced by increased number of (CD3+)T-cells, by about twice (p < 0.001) increased number of (CD4+)T-helper cells and by 68% (p < 0.001) increased number of (CD8+)T-suppressor cells. The higher increase of (CD4+)T-helper cells compared to (CD8+)T-suppressor cells caused the increased value of the (CD4+)T-helper/(CD8+)T-suppressor ratio by about 25% (p < 0.01) in the subjects exposed to S02. In contrast, a decreased number of (CD16+)NK cells by about 38% (p < 0.001) in men exposed to S02 was also observed. No changes were observed in the number of (CD19+)B-cells, as well as in the (CD3+)T/(CD8+)T-suppressor ratio. In the group exposed to S02, elevation of IgG serum levels by 23.3% (p < 0.001) was evidenced, as well as a decrease of C3c by 15.6% (p < 0.001) and C4 by 30% (p < 0.001), whereas total CIC in the serum was elevateds in same conditions by about 74% (p < 0.001). No changes were observed in the serum levels of IgA, IgM, IgE, CRP, haptoglobin, ceruloplasmin and transferrin. Significant positive correlations Irl (0.51 to 0.57) were only between S02 concentrations in air and serum concentrations of total CIC. Moreover, significant negative correlations Irl between S02 concentrations in air and leucocytes (WBC), and the determined T-cells populations and (CD19+)B-cells also were observed. In conclusion, environmental exposure to S02 can enhance proinflammatory processes in degree of exposure dependent manner and also can change some parameters of cell-mediated immunity.
The metabolism of renin-angiotensin system (RAS) is more complicated than previously expected and understanding the biological phenomena regulated by variety of angiotensin metabolites requires their precise and possibly comprehensive quantitation. Physiological concentrations of angiotensins (Ang) in biological fluids are low, therefore their accurate measurements require very sensitive and specific analytical methods. In this study we developed an accurate and reproducible method of quantitation of angiotensin metabolites through coupling of liquid chromatography and electrospray ionization - mass spectrometry (LC-ESI-MS). With this method main angiotensin metabolites (Ang I, II, III, IV, 1-9, 1-7, 1-5) can be reliably measured in organ bath of rat tissues (aorta, renal artery, periaortal adipose tissue) and in medium of cultured endothelial cells (EA.hy926), exposed to Ang I for 15 minutes, in the absence or in the presence of angiotensin converting enzyme inhibitor, perindoprilat. Presented LC-ESI-MS method proved to be a quick and reliable solution to comprehensive analysis of angiotensin metabolism in biological samples.
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