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 As^III 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 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 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-κB 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.

^{砷 (As) 以亚砷酸盐 (As III} ) 和砷酸盐 (As ^V )的形式广泛存在于环境中。氧化应激和炎症被认为是体内和体外As ^{III毒性的主要机制。}本研究的目的是调查锌 (Zn ^{2+ ) 是否能减轻由 As III}引起的鲤鱼外源性鳃毒性，并深入了解其潜在机制。鲤鱼暴露于 2.83 mg As ₂ O ₃/L 30天使超氧化物歧化酶活性降低4.0％，过氧化氢酶降低41.0％，谷胱甘肽降低19.8％，而丙二醛浓度与对照组相比增加16.4％，表明氧化应激。鲤鱼暴露于As ^III后，鳃组织中IL-6、IL-8、肿瘤坏死因子α和诱导型一氧化氮合酶等炎症标志物的表达显着增加。此外，核因子 kappa-B (NF-κB) 的磷酸化增加了 225%。基于组织病理学、抗氧化酶活性、qRT-PCR和western结果，1 mg ZnCl ₂ /L可以减轻As ^{III的毒性。}Zn ²⁺衰减 As ^III-诱导的鳃毒性，通过上调金属硫蛋白抑制细胞内氧化应激和 NF-κB 途径。因此，降低了 As ^III对鲤鱼鳃细胞的毒性作用。本研究为探索重金属对类金属对生物体的毒性作用的缓解及其作用的生物学评价提供了理论依据。