为研究水体镉(Cd)暴露对黄颡鱼(Pelteobagrus fulvidraco)鳃的组织学结构、抗氧化状态及免疫相关基因表达的影响, 将黄颡鱼分别暴露于0(对照组)、50和200 μg/L Cd水体中8周后, 取鳃进行分析.结果显示: 鳃中Cd含量随着水体Cd浓度的升高而上升; 组织学分析发现, Cd暴露组鳃出现了动脉瘤、细胞增生、鳃小片弯曲以及细胞脱落等病理变化.同时, Cd暴露导致鳃中谷胱甘肽-S-转移酶(GST)、谷胱甘肽过氧化物酶 (GPx)和抗羟自由基(AHR)的活性及过氧化氢(H2O2)的含量升高, 而过氧化氢酶(CAT)的活性及还原型谷胱甘肽(GSH)的含量下降, 但超氧化物歧化酶(SOD)的活性无显著变化.此外, Cd暴露上调了肿瘤坏死因子-α(tnf-α)、主要组织相容性复合体(mhc)、白细胞介素-10(il-10)、转化生长因子-β(tgf-β)和补体因子C3(c3)的表达,而下调了白细胞介素-1β(il-1β)、白细胞介素-8(il-8)及溶菌酶(lys)的转录水平.研究表明, Cd暴露导致黄颡鱼鳃中Cd富集, 进而诱导鳃的组织学损伤、氧化应激和免疫反应.%To investigate the effect of different Cd (0 (control), 50, and 200 μg/L Cd2+) on Yellow catfish (Pelteobagrus fulvidraco), fish were exposed for 8 weeks before analyzing the histological structure, antioxidant status and immune-related gene expression in gills. The results showed that Cd2+ exposure induced significant Cd accumulation and histological changes in gill, such as aneurism, hyperplasia, curling of lamella and cell desquamation. Meanwhile, Cd2+ increased the activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx) and anti-hydroxyl radical (AHR) as well as the content of hydrogen peroxide (H2O2), and it decreased catalase (CAT) activity and glutathione (GSH) content. However, Cd2+ had no significant effect on superoxide dismutase (SOD) activity. In addition, Cd exposure up-regulated tumor necrosis factor-a (tnf-a), major histocompatibility complex (mhc), interleukin-10 (il-10), transforming growth factor-β (tgf-β) and complement factor C3 (c3) expressions, but down-regulated interleukin-1β (il-1β), interleukin-8 (il-8) and lysozyme (lys) transcription levels. These results showed that Cd exposure resulted in the accumulation of Cd, and induced histological damage, oxidative stress and immune response of gill in yellow catfish.
展开▼
