Immune responses and protective efficacy of diet supplementation with selenium nanoparticles against cadmium toxicity in Oreochromis niloticus

俄勒冈 生物 丙二醛 过氧化氢酶 毒性 尼罗罗非鱼 免疫系统 谷胱甘肽 抗氧化剂 谷胱甘肽过氧化物酶 肿瘤坏死因子α 内分泌学 内科学 免疫学 氧化应激 生物化学 医学 渔业
作者
Nermeen M. Abu‐Elala,Mohamed Shaalan,Sara E. Ali,Nehal A. Younis
出处
期刊:Aquaculture Research [Wiley]
卷期号:52 (8): 3677-3686 被引量:36
标识
DOI:10.1111/are.15212
摘要

The present study aims to determine the effects of dietary selenium nanoparticles (Se-NPs) on growth, immune response and histopathological alterations induced by sublethal cadmium (Cd) toxicity in Nile tilapia (Oreochromis niloticus). It was carried out through two phases: in the first phase, fish were divided into two groups: a control group fed a basal diet and a treated group fed Se-NP-supplemented diet at 1 mg/kg for four weeks. Growth indices, innate immunological parameters and gene expression of interleukin (IL-1β), tumour necrosis factor (TNF-α), catalase (CAT) and insulin growth factor (IGF-1) were measured. In the second phase, fish were subdivided into four groups: G1, control, G2 was fed a control diet and exposed to Cd (5 mg/L water), G3 was fed Se-NPs-supplemented diet and G4 was fed Se-NPs-supplemented diet and exposed to Cd (5 mg/L water). Tissue samples were collected for histopathological investigation and measuring of malondialdehyde (MDA) and glutathione reduced (GSH) activity 10 days post-Cd exposure. Dietary Se-NPs increased phagocytic and lysozyme activities in the 2nd week, whereas the phagocytic index and growth indices were increased in the 4th week. IGF-1 was upregulated after 2 weeks, and TNF-α, IL-1β and CAT genes upregulated after 4 weeks. Cd caused gill hyperplasia and degenerative changes in visceral organs, elevation in MDA and attenuation in GSH activity. However, in G4 group, the histopathological alterations and antioxidant enzyme were alleviated. Thus, we conclude that dietary Se-NPs improve the growth, immunity and antioxidant power of O. niloticus and alleviate the pathological disorders induced by Cd toxicity.
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