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

Abstract

Arsenic (As) is widely present in the environment in form of arsenite (AsIII) and arsenate (AsV). 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 AsIII 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 AsIII the expression of inflammatory markers, such as interleukin-6, interleukin-8, tumor necrosis factor α and inducible nitric oxide synthase in gill tissue were significantly increased. In addition, the phosphorylation of nuclear factor kappa-B (NF-κB) was increased by 225%. 1 mg ZnCl2/L can relieve the toxicity of AsIII based on histopathology, antioxidase activity, qRT-PCR and western results. Zn2+ attenuated AsIII-induced gill toxicity that suppressed intracellular oxidative stress and NF-κB pathway by an upregulation of metallothionein. Therefore, the toxic effect of AsIII 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.