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微囊藻毒素-RR通过产生活性氧并导致线粒体损伤来诱导鱼类淋巴细胞凋亡。

Microcystin-RR induces apoptosis in fish lymphocytes by generating reactive oxygen species and causing mitochondrial damage.

作者信息

Zhang H, Zhang J, Chen Y, Zhu Y

机构信息

College of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310028, PR China.

出版信息

Fish Physiol Biochem. 2008 Dec;34(4):307-12. doi: 10.1007/s10695-007-9189-7. Epub 2007 Nov 7.

Abstract

Microcystin-RR (MCRR), a very widespread toxic microcystin in China, has previously been proved to induce sensitive apoptosis in Carassius auratus lymphocytes in vitro. This study focused on the role of intracellular Ca(2+), mitochondrial membrane potential, reactive oxygen species, and intracellular ATP in the mechanism of MCRR-induced apoptotic toxicity to fish lymphocytes. Compared with controls, administration of MCRR (10 nmol L(-1)) caused a massive calcium influx resulting in elevation of reactive oxygen species (ROS), rapid disruption of mitochondrial membrane potential (DeltaPsim), and depletion of ATP. This study provided a possible mechanism for the cytotoxicity of microcystins to fish lymphocytes.

摘要

微囊藻毒素-RR(MCRR)是中国一种广泛存在的有毒微囊藻毒素,先前已被证明可在体外诱导鲫鱼淋巴细胞发生敏感凋亡。本研究聚焦于细胞内钙离子、线粒体膜电位、活性氧和细胞内ATP在MCRR诱导鱼类淋巴细胞凋亡毒性机制中的作用。与对照组相比,给予MCRR(10 nmol L⁻¹)导致大量钙离子内流,从而导致活性氧(ROS)升高、线粒体膜电位(ΔΨm)迅速破坏以及ATP耗竭。本研究为微囊藻毒素对鱼类淋巴细胞的细胞毒性提供了一种可能的机制。

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