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Oxidative stress and histopathological alterations in liver of Cyprinus carpio L. induced by intraperitoneal injection of microcystin-LR

机译:腹腔注射微囊藻毒素-LR诱导鲤鱼肝脏的氧化应激及组织病理学改变

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Microcystins (MCs) are a group of cyclic heptapeptide hepatotoxic peptides produced by cyanobacteria. Microcystins-LR (MC-LR) can inhibit the activities of protein phosphatase type 1 and type 2A (PP1 and PP2A) and induce excessive production of reactive oxygen species (ROS). However, the detailed toxicological mechanism involving oxidative stress in carp (Cyprinus carpio L.) remains largely unclear. In our present study, the effects of sublethal intraperitoneal doses of MC-LR on the oxidative stress and pathological changes in carp liver were investigated. No significant changes of xanthine oxidase were observed, suggesting it might not contribute to over-production of ROS in the liver of fish during 48 h exposure to sublethal intraperitoneal doses of MC-LR. Superoxide dismutase activity in the 50 mu g kg(-1) group was significantly induced at 1-24 h. The strongest inhibition of the catalase activity was shown at 48 h after 120 mu g kg(-1) MC-LR exposure, with an inhibition rate of 33.7 % compared to the control group. In general, a significant depletion of intracellular reduced glutathione was found at 5-12 h after 50 and 120 mu g kg(-1) MC-LR exposure, which was mainly due to the conjugation reaction to MC-LR catalyzed by glutathione-S-transferase and its subsequent excretion. Oxidative damages induced by MC-LR were evidenced by the significant elevation in malondialdehyde levels. In addition, a series of histopathological alterations in fish livers were observed, and the most severe hepatic injuries were found at 5-12 h, which could contribute to the efflux of intracellular GSH. Our study further supports the important role of oxidative stress involved in MC-LR induced liver injury in aquatic organisms.
机译:微囊藻毒素(MCs)是由蓝细菌产生的一组环状七肽肝毒性肽。微囊藻毒素-LR(MC-LR)可以抑制1型和2A型蛋白磷酸酶(PP1和PP2A)的活性,并诱导过量产生活性氧(ROS)。但是,关于鲤鱼(Cyprinus carpio L.)氧化应激的详细毒理机制仍不清楚。在本研究中,研究了腹膜下亚致死剂量的MC-LR对鲤鱼肝脏氧化应激和病理变化的影响。黄嘌呤氧化酶未见明显变化,表明在暴露于亚致死性腹膜内剂量的MC-LR 48小时后,可能不会导致鱼肝中ROS的过量产生。 50微克kg(-1)组中的超氧化物歧化酶活性在1-24小时被显着诱导。在120μg kg(-1)MC-LR暴露后48小时,对过氧化氢酶活性的抑制作用最强,与对照组相比,抑制率为33.7%。通常,在50和120μg kg(-1)MC-LR暴露后5-12小时发现细胞内还原型谷胱甘肽显着减少,这主要是由于谷胱甘肽-S催化与MC-LR的结合反应-转移酶及其随后的排泄。丙二醛水平明显升高证明了MC-LR引起的氧化损伤。此外,在鱼肝中观察到一系列组织病理学改变,在5-12 h发现最严重的肝损伤,这可能有助于细胞内GSH的外流。我们的研究进一步支持了氧化应激在MC-LR引起的水生生物肝损伤中的重要作用。

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