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首页> 外文期刊>Environmental Science and Pollution Research >Vitamin C modulates cadmium-induced hepatic antioxidants' gene transcripts and toxicopathic changes in Nile tilapia, Oreochromis niloticus
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Vitamin C modulates cadmium-induced hepatic antioxidants' gene transcripts and toxicopathic changes in Nile tilapia, Oreochromis niloticus

机译:维生素C调节镉诱导的肝脏抗氧化剂的基因转录物和尼罗拉氏菌,奥海罗米斯尼洛尼亚的毒性变化

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Cadmium (Cd) is one of the naturally occurring heavy metals having adverse effects, while vitamin C (l-ascorbic acid) is an essential micronutrient for fish, which can attenuate tissue damage owing to its chain-breaking antioxidant and free radical scavenger properties. The adult Nile tilapia fish were exposed to Cd at 5 mg/l with and without vitamin C (500 mg/kg diet) for 45 days in addition to negative and positive controls fed with the basal diet and basal diet supplemented with vitamin C, respectively. Hepatic relative mRNA expression of genes involved in antioxidant function, metallothionein (MT), glutathione S-transferase (GST-alpha 1), and glutathione peroxidase (GPx1), was assessed using real-time reverse transcription polymerase chain reaction (RT-PCR). Hepatic architecture was also histopathologically examined. Tilapia exposed to Cd exhibited upregulated antioxidants' gene transcript levels, GST-ai(0)1, GPx1, and MT by 6.10-, 4.60-, and 4.29-fold, respectively. Histopathologically, Cd caused severe hepatic changes of multifocal hepatocellular and pancreatic acinar necrosis, and lytic hepatocytes infiltrated with eosinophilic granular cells. Co-treatment of Cd-exposed fish with vitamin C overexpressed antioxidant enzyme-related genes, GST-ai(0)1 (16.26-fold) and GPx1 (18.68-fold), and maintained the expression of MT gene close to control (1.07-fold), averting the toxicopathic lesions induced by Cd. These results suggested that vitamin C has the potential to protect Nile tilapia from Cd hepatotoxicity via sustaining hepatic antioxidants' genes transcripts and normal histoarchitecture.
机译:镉(Cd)是具有不良反应的天然存在的重金属中的一种,而维生素C(L-抗坏血酸)为鱼必需的微量营养素,其可由于其断链抗氧化剂和自由基清除剂性能衰减的组织损伤。罗非鱼成年尼罗河暴露于镉在5毫克/升用和不用除了负,并用基础饮食和基础日粮阳性对照45天分别补充有维生素C,维生素C(500毫克/千克饮食) 。参与抗氧化功能,金属硫蛋白(MT),谷胱甘肽S-转移酶(GST-α1),谷胱甘肽过氧化物酶(GPX1)基因的肝相对mRNA表达,使用实时反转录聚合酶链反应进行了评估(RT-PCR) 。肝架构也病理学检查。罗非鱼暴露于镉表现出上调抗氧化剂基因转录物水平,GST-AI(0)1,GPX1,和MT通过6.10-,4.60-,和4.29倍,分别。病理组织学检查,镉引起的肝细胞多灶性和胰腺腺泡坏死,并有嗜酸性颗粒细胞浸润裂解肝细胞的严重肝功能的变化。镉暴露鱼维生素C的共处理过表达抗氧化剂酶相关基因,GST-AI(0)1(16.26倍)和GPX1(18.68倍),并保持MT基因接近控制的表达(1.07倍),从而避免了toxicopathic病变镉诱导。这些结果表明,维生素C具有通过维持肝的抗氧化剂的基因转录物和正常histoarchitecture保护尼罗罗非鱼从镉肝毒性的潜力。

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