YANG Huan, WANG Su-hua, SU Xin, GAO Yan-rong. Effects of sodium arsenite on inflammatory cytokines and oxidative stress in male rats[J]. Journal of Environmental and Occupational Medicine, 2017, 34(6): 542-544. DOI: 10.13213/j.cnki.jeom.2017.16812
Citation: YANG Huan, WANG Su-hua, SU Xin, GAO Yan-rong. Effects of sodium arsenite on inflammatory cytokines and oxidative stress in male rats[J]. Journal of Environmental and Occupational Medicine, 2017, 34(6): 542-544. DOI: 10.13213/j.cnki.jeom.2017.16812

Effects of sodium arsenite on inflammatory cytokines and oxidative stress in male rats

  • Objective To investigate the effects of sodium arsenite on serum inflammatory cytokine and oxidative stress levels in male rats.

    Methods Thirty-two specific-pathogen-free healthy male SD rats were randomly divided into four groups: control group, low dose, medium dose, and high dose groups, with eight rats in each group. The three exposure groups were intoxicated by 10, 100, and 1 000 μg/L NaAsO2 in drinking water, respectively, while the control group was given ultrapure water for free drinking. All the rats were sacrificed after 28 days. The levels of granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-10 (IL-10), nicotinanmide adenine dinucleotide phosphate (NADPH) oxidase, reactive oxygen species (ROS), total antioxidant capacity, and nitric oxide (NO) were determined by enzyme-linked immunosorbent assay.

    Results Sodium arsenite exposed rats showed significantly higher GM-CSF expression levels than the control group (P < 0.05), and the 1 000 μg/L group had the highest GM-CSF expression level. The anti-inflammatory cytokine IL-10 levels were lower in all exposure groups than in the control group (P < 0.05). The 1 000 μg/L group showed a higher ROS level than the control group (P < 0.05). NO expression levels were increased in all exposure groups compared with the control group (P < 0.05), and there was a dose-response relationship.

    Conclusion Sodium arsenite exposure in male rats could lead to inflammatory injury and oxidative stress injury, and the mechanism may be related to elevated NO and reduced IL-10.

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