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Effects of ammonia exposure on apoptosis, oxidative stress and immune response in pufferfish (Takifugu obscurus)

机译:氨水暴露对河豚(暗纹东方鱼)细胞凋亡,氧化应激和免疫应答的影响

摘要

Ammonia is one of major environmental pollutants in the freshwater aquatic system that affects the survival and growth of organisms. In the present study, we investigated the effects of ammonia exposure on apoptosis, oxidative stress and immune response in pufferfish (Takifugu obscurus). Fish were exposed to various concentrations of ammonia (0, 1.43, 3.57, 7.14 mM) for 72 h. The date showed that ammonia exposure could induce intracellular reactive oxygen species (ROS), interrupt intracellular Ca2+ (cf-Ca2+) homeostasis, and subsequently lead to DNA damage and cell apoptosis. To test the apoptotic pathway, the expression patterns of some key apoptotic related genes including P53, Bax Bcl2, Caspase 9, Caspase 8 and Caspase 3 in the liver were examined. The results showed that ammonia stress could change these genes transcription, associated with increasing of cell apoptosis, suggesting that the P53-Bax-Bcl2 pathway and caspase-dependent apoptotic pathway could be involved in cell apoptosis induced by ammonia stress. In addition, ammonia stress could induced up-regulation of inflammatory cytokines (BAFF, TNF-alpha, IL-6 and IL-12) transcription, indicating that innate immune system play important roles in ammonia-induced toxicity in fish. Furthermore, the gene expressions of antioxidant enzymes (Mn-SOD, CAT, GPx, and GR) and heat shock proteins (HSP90 and HSP70) in the liver were induced by ammonia stress, suggesting that antioxidant system and heat shock proteins tried to protect cells from oxidative stress and apoptosis induced by ammonia stress. Our results will be helpful to understand the mechanism of aquatic toxicology induced by ammonia in fish. (C) 2015 Elsevier B.V. All rights reserved.
机译:氨是淡水水生系统中影响有机物生存和生长的主要环境污染物之一。在本研究中,我们调查了氨暴露对河豚鱼(Takifugu obscurus)细胞凋亡,氧化应激和免疫反应的影响。将鱼暴露于各种浓度的氨(0、1.43、3.57、7.14 mM)72小时。日期表明,氨暴露可诱导细胞内活性氧(ROS),中断细胞内Ca2 +(cf-Ca2 +)稳态,并随后导致DNA损伤和细胞凋亡。为了测试凋亡途径,检查了一些关键的凋亡相关基因在肝脏中的表达模式,包括P53,Bax Bcl2,Caspase 9,Caspase 8和Caspase 3。结果表明,氨胁迫可以改变这些基因的转录,并伴随细胞凋亡的增加,提示P53-Bax-Bcl2途径和胱天蛋白酶依赖性凋亡途径可能与氨胁迫诱导的细胞凋亡有关。此外,氨胁迫可能诱导炎症细胞因子(BAFF,TNF-α,IL-6和IL-12)的转录上调,表明先天免疫系统在氨诱导的鱼类毒性中起重要作用。此外,氨应激可诱导肝脏中抗氧化酶(Mn-SOD,CAT,GPx和GR)和热休克蛋白(HSP90和HSP70)的基因表达,表明抗氧化系统和热休克蛋白试图保护细胞。氧化应激和氨胁迫诱导的细胞凋亡。我们的研究结果将有助于了解鱼类中氨引起的水生毒理学机理。 (C)2015 Elsevier B.V.保留所有权利。

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