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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调节尼罗罗非鱼,尼罗罗非鱼中镉诱导的肝抗氧化剂的基因转录和毒理性变化

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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)是自然产生的具有不利影响的重金属之一,而维生素C(1-抗坏血酸)是鱼类必需的微量营养素,由于其具有断链抗氧化剂和自由基清除剂的特性,因此可以减轻组织损伤。除了分别饲喂基础饮食和补充维生素C的基础饮食的阴性和阳性对照外,成年尼罗罗非鱼鱼分别在含和不含维生素C(500 mg / kg饮食)的情况下以5 mg / l的镉暴露45天。 。使用实时逆转录聚合酶链反应(RT-PCR)评估了抗氧化功能,金属硫蛋白(MT),谷胱甘肽S-转移酶(GST-alpha 1)和谷胱甘肽过氧化物酶(GPx1)相关基因的肝相对mRNA表达。 。肝结构也进行了组织病理学检查。暴露于Cd的罗非鱼表现出抗氧化剂的基因转录水平上调,分别是GST-ai(0)1,GPx1和MT的6.10-,4.60-和4.29-倍。在组织病理学上,Cd引起严重的肝脏多灶性肝细胞和胰腺腺泡坏死变化,溶血性肝细胞浸润了嗜酸性粒细胞。与维生素C过表达的抗氧化酶相关基因GST-ai(0)1(16.26倍)和GPx1(18.68倍)共同处理镉暴露的鱼类,并保持MT基因的表达接近对照(1.07) -倍),避免了Cd引起的中毒病变。这些结果表明,维生素C可以通过维持肝脏抗氧化剂的基因转录物和正常的组织结构来保护尼罗罗非鱼免受Cd肝毒性。

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