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Changing levels of selenium and zinc in cadmium-exposed workers: probable association with the intensity of inflammation

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Abstract

Inflammation is a response mediated by multiple cytokines, such as IL-6, IL-10 and TNF-α. Cadmium (Cd) has been involved in the etiopathogenesis of many diseases via inflammation. Selenium (Se) and zinc (Zn) play a pivotal role in maintaining many physiological functions of cells as well as inhibiting Cd-induced cytotoxicity. This study investigated the anti-inflammatory effects of Se and Zn in cadmium-exposed workers by measuring the levels of IL-6, IL-10 and TNF-α cytokines in 68 control and 91 Cd-exposed subjects. Blood samples were obtained from each participant for immunological, toxicological and routine analysis. All samples were digested by microwave oven and analysed by inductively coupled plasma mass spectrometry (ICP-MS). IL-6, IL-10 and TNF-α cytokine levels were found to be statistically different (p < 0.001) between the control and Cd-exposed groups (23.50 ± 7.70 pg/mL vs. 69.05 ± 19.06 pg/mL; 28.61 ± 9.83 pg/mL vs. 51.79 ± 11.77 pg/mL; 3.44 ± 1.14 pg/mL vs. 5.79 ± 1.04 pg/mL, respectively). High positive correlations were found between Cd levels of participants and IL-6, IL-10, TNF-α and CRP levels (r = 0.568, r = 0.615, r = 0.614 and r = 0.296, respectively, p < 0.01). In terms of the regression analysis results, there were significant effects of Cd on IL-6, IL-10 and TNF-α levels (p < 0.05). The Cd, Zn and Se levels between control and exposed group were significantly different [0.26 ± 0.15 µg/L vs. 3.36 ± 1.80 µg/L; 143.91 ± 71.13 µg/dL vs. 121.09 ± 59.88 µg/dL; 92.98 ± 17.03 µg/L vs. 82.72 ± 34.46 µg/L (p < 0.001, p < 0.03, p < 0.015), respectively]. In conclusion, increasing levels of Se and Zn decreases the intensity of inflammation as measured by IL-6, IL-10 and TNF-α levels.

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Correspondence to Vugar Ali Turksoy.

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Turksoy, V.A., Tutkun, L., Gunduzoz, M. et al. Changing levels of selenium and zinc in cadmium-exposed workers: probable association with the intensity of inflammation. Mol Biol Rep 46, 5455–5464 (2019). https://doi.org/10.1007/s11033-019-05001-4

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