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蔡荣, 郭赛男, 郑家浪*. Cd2+暴露对斑马鱼肝脏和卵巢抗氧化和免疫系统的影响及蓝LED光预暴露的保护作用[J]. 生态毒理学报, 2018, 13(1): 169-178
Cd2+暴露对斑马鱼肝脏和卵巢抗氧化和免疫系统的影响及蓝LED光预暴露的保护作用
Effect of Cadmium Exposure on Antioxidant and Immune Responses and the Ameliorative Role of Blue LEDs Pre-exposure in the Liver and Ovary of Zebrafish
投稿时间:2017-05-15  修订日期:2017-06-28
DOI:10.7524/AJE.1673-5897.20170515002
中文关键词:  光谱预暴露    斑马鱼  氧化应激  免疫毒性  金属暴露  Nrf2  NF-κB
英文关键词:spectra acclimation  Cd  zebrafish  oxidative stress  immunotoxicity  metal exposure  Nrf2  NF-κB
基金项目:国家自然科学基金青年科学基金项目(41606122)
作者单位
蔡荣, 郭赛男, 郑家浪* 浙江海洋大学 海洋科学学院舟山 316000 
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中文摘要:
      本研究探讨了急性镉暴露(Cd2+)对斑马鱼抗氧化和免疫系统的影响及蓝LED光源(LDB)预暴露的缓解作用。斑马鱼均分为2组,分别用白炽灯和LDB处理4周(辐照度为0.9 W m-2)。4周后每组再分为2个小组,分别在白炽灯下用0和0.97 mg L-1 Cd2+的水体处理4 d。结果表明:Cd2+暴露导致肝脏和卵巢丙二醛(MDA)和一氧化氮(NO)含量的显著升高。在肝脏中,Cd2+暴露下调了铜锌超氧化物歧化酶(Cu/Zn-SOD)和过氧化氢酶(CAT)的酶活和mRNA表达水平,上调了环氧化酶2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达和酶活。在卵巢中,Cd2+导致Cu/Zn-SOD和CAT的表达,CAT、COX-2和iNOS的酶活显著升高。在卵巢中,LDB预暴露可显著缓解Cd2+引起的MDA和NO含量、Cu/Zn-SOD的表达、CAT的表达和酶活、COX-2和iNOS的酶活的升高。在肝脏中,LDB预暴露不能影响Cd2+引起的MDA和NO含量的升高,但是显著缓解了Cd2+引起的Cu/Zn-SOD和CAT表达和酶活的下降和COX-2和iNOS表达的升高。在这些过程中,核转录相关因子2(Nrf2)和核转录因子-κB(NF-κB)与其目标基因的表达及其抑制因子Kelch样ECH联合蛋白1(Keap1a和Keap1b)和抑制蛋白激酶(IκBαa和IκBαb)显示了紧密的关联性。综上结果表明, 斑马鱼急性Cd2+暴露后,机体处于氧化应激状态, 导致肝脏和卵巢氧化性损伤和炎症的产生,而LDB预暴露能够改善机体这种不利状态。这个过程可能分别涉及Nrf2和NF-κB诱导的抗氧化和免疫系统。
  
AuthorAffiliation
Cai Rong, Guo Sainan , Zheng Jialang*College of Marine Science and Technology, Zhejiang Ocean University, Zhoushan 316000, China
英文摘要:
      The present hypothesis is that blue light emitting diodes (LDB) pre-exposure will lead to amelioration of Cd-induced oxidative stress and immunotoxicity in zebrafish. To the end, zebrafish were pre-exposed to a white fluorescent bulb or LDB at an irradiance of 0.9 W m-2 for 4 weeks, and then exposed to 0 and 0.97 mg L-1 Cd for 4 days, respectively. Cd exposure alone increased the levels of malondialdehyde (MDA) and nitric oxide (NO) in liver and ovary. In liver, Cd exposure alone down-regulated copper and zinc superoxide dismutase (Cu/Zn-SOD) and catalase (CAT) and up-regulated inducible nitric oxide synthase (iNOS) and ciclooxigenase-2 (COX-2) at mRNA and activity levels. In ovary, Cd exposure alone increased mRNA levels of Cu/Zn-SOD and activity levels of CAT, COX-2 and iNOS. However, LDB acclimation mitigated Cd-induced oxidative stress and inflammatory responses in ovary by reducing MDA and NO levels and down-regulating related genes at mRNA and/or activity levels. The mitigative effect was not observed in liver because there was no difference in MDA and NO levels between Cd exposure and Cd exposure with LDB acclimation. However, LDB acclimation mitigated Cd-induced disturbance of Cu/Zn-SOD, CAT, iNOS, and COX-2 at mRNA and/or activity levels. Pearson correlations between mRNA expression levels of nuclear transcription factor κB (NF-κB) and E2-related factor (Nrf2) and their target genes as well as inhibitors Kelch-like-ECH-associated protein 1 (Keap1a and Keap1b) and κBα (IκBαa and IκBαb) were also observed in the process. In conclusion, we demonstrated for the first time LDB acclimation could protect against Cd-induced oxidative stress and immunotoxicity, possibly involving Nrf2 and NF-κB signaling pathways in fish.
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