Arsenic (III) induces oxidative stress and inflammation in the gills of common carp, which is ameliorated by zinc (II)

Arsenic (As) is widely present in the environment in form of arsenite (As-III) and arsenate (As-V). Oxidative stress and inflammation are believed to be the dominant mechanisms of AsIII toxicity in vivo and in vitro. The aim of this study was to investigate whether zinc (Zn2+) alleviates exogenous gill toxicity in carp induced by As-III and to gain insight into the underlying mechanisms. Exposure of carp to 2.83 mg As2O3/L for 30 days reduced superoxide dismutase activity by 4.0%, catalase by 41.0% and glutathione by 19.8%, while the concentration of malondialdehyde was increased by 16.4% compared to the control group, indicating oxidative stress. After the exposure of carp to As-III the expression of inflammatory markers, such as interleukin-6, interleukin-8, tumor necrosis factor alpha and inducible nitric oxide synthase in gill tissue were significantly increased. In addition, the phosphorylation of nuclear factor kappa-B (NF-kappa B) was increased by 225%. 1 mg ZnCl2/L can relieve the toxicity of As-III based on histopathology, antioxidase activity, qRT-PCR and western results. Zn2+ attenuated As-III-induced gill toxicity that suppressed intracellular oxidative stress and NF-kappa B pathway by an upregulation of metallothionein. Therefore, the toxic effect of As(III )on the gill cells of carp was reduced. This study provides a theoretical basis for exploring the alleviation of the toxic effects of metalloids on organisms by heavy metals and the biological assessment of the effects.