虎杖提取物对尼罗罗非鱼脂肪肝的干预作用

为探究虎杖提取物对尼罗罗非鱼(Oreochromis niloticus)脂肪肝的干预作用,选取120尾健康尼罗罗非鱼,随机分为4组,分别投喂基础饲料(正常组,粗脂肪6%),高脂饲料(高脂组,粗脂肪21%),以及含2.5、5 g/kg虎杖提取物的高脂饲料。饲养60 d后,采集尼罗罗非鱼血液和肝组织,并测定血脂水平、抗氧化状态和基因表达。结果显示:与正常组相比,高脂饲料投喂显著提高了尼罗罗非鱼血脂水平、引起了氧化应激和炎症反应、最终导致了肝损伤发生。与高脂组相比,虎杖提取物组明显抑制了血清血脂水平和谷丙转氨酶(GPT)活性上升,以及肝组织中超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和谷胱甘肽(GSH)水平的下降;同时虎杖提取物显著降低了肝组织中丙二醛(MDA)和肝脂肪含量;此外,基因表达数据显示,虎杖提取物显著阻碍了白细胞介素-1β(IL-1β)的上调和过氧化物酶体增殖物激活受体α(PPAR-α)下调。结果表明虎杖提取物可明显缓解高脂饲料引起的尼罗罗非鱼脂肪性肝损伤。     

氧化应激对鲤抗氧化状态和免疫功能的影响

为探讨氧化应激对鲤抗氧化状态和免疫功能的影响,本实验以H_2O_2作为活性氧自由基(ROS),将鲤暴露于不同浓度的H_2O_2(0、0.25、0.50和1.00 mmol/L)中,诱导鲤产生氧化应激反应。连续暴露7 d后,采集鲤血液和肝组织,以检测相关生化指标以及基因表达量的变化。结果显示,与空白对照组(0 mmol/L)相比,随着H_2O_2浓度的升高,血清葡萄糖(GLU)、皮质醇(cortisol)和乳酸(LA)含量显著升高;而碱性磷酸酶(AKP)和酸性磷酸酶(ACP)活性仅在1.00 mmol/L H_2O_2处理组中显著高于其他实验组。氧化应激参数显示,与空白对照组(0 mmol/L)相比,0.50和1.00 mmol/L H2O2处理显著降低血清过氧化氢酶(CAT)活性,而提高还原型谷胱甘肽(GSH)、丙二醛(MDA)和总抗氧化能力(T-AOC)水平;在肝脏组织中,1.00 mmol/L H_2O_2处理显著降低了GSH含量,促进了MDA生成。基因表达结果显示,与空白对照组相比,1.00 mmol/L H2O2处理组显著上调了肝脏组织中cyp1a表达,而下调了cyp1b表达;同时0.50和1.00 mmol/L H2O2处理显著上调了hsp70、hsp90、c3、c-lyz和hep的表达。研究表明,氧化应激暴露可诱导鲤产生明显应激反应和脂质过氧化,降低机体抗氧化能力并激发免疫应答反应。     

纳米ZnO和常规ZnO、ZnSO4对斑马鱼毒性效应的比较

为比较纳米ZnO、常规ZnO和ZnSO_4对斑马鱼氧化应激毒性的强弱,探究纳米ZnO的毒性作用与其释放的Zn2+和本身特性的关系,研究了纳米ZnO、常规ZnO、ZnSO_4对斑马鱼肝脏、肠、鳃组织中抗氧化酶活性及炎症凋亡基因表达的影响。实验将斑马鱼分别暴露于纳米ZnO、常规ZnO、ZnSO_4水体中,在4、24和96 h后,用分光光度法检测斑马鱼肝脏、肠、鳃中过氧化氢酶(CAT)、谷胱甘肽(GSH)、谷胱甘肽硫转移酶(GST)、活性氧自由基(ROS)的变化;采用荧光定量PCR技术,测定实验组中肝脏、肠和鳃中Bax、Bcl-2、TNF-α及IL-6的mRNA相对表达量。结果显示,纳米ZnO、常规ZnO、ZnSO_4均引起斑马鱼各组织的氧化应激反应,且使组织中凋亡基因和炎症基因表达水平发生变化,激活生物体内的细胞坏死和细胞凋亡途径,引起细胞死亡或机体炎症,其中纳米ZnO的致氧化损伤作用最强。研究表明,纳米ZnO对斑马鱼的氧化应激毒性强于常规ZnO和ZnSO_4,而纳米颗粒本身特性是导致纳米ZnO毒性作用的主要原因。     

不同碳水化合物水平对大口黑鲈鳃组织结构、抗氧化能力和免疫能力的影响

为了探究高碳水化物对大口黑鲈鳃组织结构的完整性、抗氧化能力和免疫能力的影响,设计3种不同碳水化物水平的等氮等脂饲料：7%(L组),12%(M组),17%(H组)。选取初始体重为4.0±0.2g的大口黑鲈360尾,饲喂8周。通过组织切片,抗氧化和免疫酶活的测定及mRNA的表达研究,结果表明：H组能够导致鳃小片基部细胞增生、融合,上皮细胞脱落；H组和M组的丙二醛(MDA)含量显著高于L组(P<0.05)；鳃组织的超氧化物歧化酶(SOD)、过氧化物酶(CAT)在H组和M组显著低于L组(P<0.05)；H组和M组抗氧化酶(CAT,GPX,SOD1,SOD2,SOD3a,SOD3b) mRNA水平也要显著低于L组(P<0.05)；H组和M组酸性磷酸酶(AKP),碱性磷酸酶(ACP)和溶菌酶(LZM)也要显著低于L组(P<0.05)；H组和M组免疫相关基因(IL-1β,IL-10,IL-15,TNF-α和TGF-1β)和抗菌肽(hepcidin-1和hepcidin-2)mRNA水平显著低于L组mRNA水平(P<0.05)；H组凋亡相关的基因(caspase-3,caspase-8,caspase-9)的mRNA水平显著高于L组和M组(P<0.05)；H组的ocluding和claudin-7 mRNA水平显著低于L组和M组(P<0.05)。研究表明：在本实验条件下,饲喂高碳水化物饲料会损伤大口黑鲈鳃组织结构,降低抗氧化能力和免疫能力。     

银杏叶提取物对鲤生长性能、抗氧化功能和免疫相关基因表达的影响

为探讨日粮中添加不同水平的银杏叶提取物(Ginkgo bioba extract, GBE)对鲤(Cyprinus carpio)生长性能、血清生化指标、抗氧化功能、细胞色素酶以及免疫相关基因表达的影响, 在基础饲料中分别添加不同含量的银杏叶提取物[0 (对照组)、0.5 g/kg、1.0 g/kg、5.0 g/kg]投喂鲤 60 d。饲喂实验结束后, 称重并采集血液、肝脏、肠道、 鳃和肌肉组织, 检测相关生化指标以及基因表达的变化。结果表明: 与对照组相比, 饲料中添加不同水平 GBE 对鲤生长性能和饵料系数均未产生显著影响(P>0.05)。血清生化数据显示: 饲料中添加 GBE 显著提高了总蛋白(TP) 含量, 而降低了葡萄糖(Glu)和皮质醇(cortisol)水平(P<0.05), 但对总胆固醇(TC)、甘油三酯(TG)、谷丙转氨酶(ALT) 和谷草转氨酶(AST)含量无显著影响(P>0.05)。抗氧化参数表明: 与对照组相比, 日粮中添加 GBE 对血清、肝脏、 肠道、鳃和肌肉中丙二醛(MDA)含量无显著影响(P>0.05), 但肝脏中总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD) 和过氧化氢酶(CAT)活性、以及还原型谷胱甘肽(GSH)含量均显著升高。同时, 1.0 g/kg GBE 显著提高了肠道和鳃 T-AOC 含量(P<0.05); 5.0 g/kg GBE 显著提高了鳃 GSH 含量(P<0.05)。基因表达结果显示: 与对照组相比, 饲料中添加 GBE 能显著诱导肝脏和肠道中 cyp3a 基因表达, 而下调 cyp1a 和 cyp1b 基因表达; 同时, 肝脏和肠道中免疫相关基因(c3 和 c-lyz)表达量在 1.0 g/kg GBE 添加组中显著上调(P<0.05)。综上所述, GBE 作为饲料添加剂不能改善鲤的生长性能和饵料系数, 但可以增强鲤的抗应激、抗氧化能力和免疫相关基因的表达, 并且未对鲤产生肝毒性, 鲤饲料中 GBE 建议添加量为 1.0 g/kg。     

饲料中添加姜黄素对尼罗罗非鱼幼鱼生长和四氯化碳诱导肝损伤的影响

本试验旨在研究饲料中姜黄素对尼罗罗非鱼(Oreochromis niloticus)幼鱼生长性能的影响和对四氯化碳(CCl_4)诱导鱼体急性肝损伤的保护作用,为筛选治疗鱼类肝脏综合征的绿色药物提供理论依据。在基础饲料中分别添加不同水平(0、15 mg/kg、30 mg/kg、60 mg/kg、120 mg/kg和240 mg/kg)的姜黄素,连续饲喂鱼体8周后进行采样,探讨姜黄素对尼罗罗非鱼生长的影响,并采用CCl_4诱导鱼体急性肝损伤,72 h后采集血液和肝组织,检测相关抗氧化指标以及肝组织切片的变化。结果显示,饲料中添加60 mg/kg和120 mg/kg姜黄素可显著增加鱼体的增重率和特定生长率(P0.05);当罗非鱼经CCl_4诱导72 h后,60 mg/kg和120 mg/kg姜黄素组的血浆谷草转氨酶(GOT)、谷丙转氨酶(GPT)活力和丙二醛(MDA)含量显著低于对照组(P0.05),而血浆总蛋白(TP)、白蛋白(ALB)、谷胱甘肽(GSH)、血浆总抗氧化能力(T-AOC)、肝超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力却显著高于对照组(P0.05);姜黄素在一定程度上可保护鱼体肝不受损伤,且以添加120 mg/kg水平时效果最佳。综上,饲料中添加60～120 mg/kg姜黄素可促进尼罗罗非鱼幼鱼生长性能的提高,而当饲料中添加120 mg/kg姜黄素时,对其肝的保护作用最强,可有效地抑制肝组织的脂质过氧化。     

低分子壳聚糖对罗非鱼肝组织抗氧化能力和肝脂含量影响的研究

采用单因子浓度梯度法,研究低分子壳聚糖(SMW-chitosan )对尼罗罗非鱼(Tilapia niloticn)肝组织抗氧化能力和肝脂含量的影响实验发现．0．25％低分子壳聚糖能显著提高罗非鱼肝组织抗超氧阴离f自由基和超氧化物岐化酶(SOD)浓度。适宜剂量的低分子壳聚精可降低罗非鱼的肝脂含量．其中O．50％低分子壳聚糖的降肝脂效果最为显著。实验表明,适宜剂量的壳聚糖可有效地提高罗非鱼的肝组织抗氧化能力．降低肝脏的脂肪含量。     

鱼腥草对无乳链球菌引起吉富罗非鱼肝脏损伤的修复作用

为探讨池塘种植鱼腥草对无乳链球菌引起吉富罗非鱼肝脏损伤的修复作用,在养殖池塘中分别种植0%(对照组)、5%、10%和15%池塘面积的鱼腥草,养殖90 d后进行无乳链球菌人工感染,分别在感染后0、24、48和72 h采集吉富罗非鱼肝脏,进行肝脏生化、抗氧化性能、组织病理和热休克蛋白70基因(HSP 70)表达研究。结果显示,感染后48和72 h对照组肝脏谷丙转氨酶(ALT)和谷草转氨酶(AST)活性最高,种植鱼腥草各组吉富罗非鱼肝脏ALT活性在感染前后均无显著性变化,感染后72 h,10%组吉富罗非鱼肝脏AST活性已恢复到感染前水平。抗氧化指标显示,种植鱼腥草能减缓链球菌感染引起吉富罗非鱼肝脏总抗氧化能力(T-AOC)下降,显著提高肝脏中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)和一氧化氮合酶(NOS)等抗氧化酶的活性,增加自由基清除能力,减少脂质过氧化丙二醛(MDA)的产生。组织病理学观察显示,对照组吉富罗非鱼感染后48 h肝窦明显淤血,肝索排列紊乱,肝细胞脂肪变性,而各种植鱼腥草组吉富罗非鱼在感染后仅表现为肝细胞明显嗜酸,肝窦轻度扩张。定量PCR结果显示,每组吉富罗非鱼肝脏HSP 70表达量在感染后都显著升高,感染后各时间点对照组吉富罗非鱼肝脏的HSP 70表达量均显著高于鱼腥草种植组。研究表明,种植鱼腥草能显著改善链球菌感染所造成的吉富罗非鱼肝脏AST和ALT上升,提高抗氧化应激能力,减轻链球菌感染引起的病理损伤;吉富罗非鱼通过肝脏HSP 70高表达促进受损蛋白质的早期修复与降解,种植鱼腥草具有抗炎作用和提高鱼体抵御病原菌的能力。     

叶下珠对罗非鱼肝损伤及免疫功能的影响

在罗非鱼Oreochromis niloticus基础饲料中添加叶下珠Phyllanthus urinaria水提物0.5%、1.0%和1.5%连续饲喂7 d,研究了叶下珠对罗非鱼肝损伤及免疫功能的影响,通过CuSO4.5H2O中毒造模、采血,检测鱼血清中的肝损伤指标(ALT、AST、ADA、LDH)和免疫指标(AKP、ACP、MPO、溶菌酶)。结果显示,各添加组的肝损伤指标、免疫指标与对照组相比,差异极显著(P0.01),而各添加组间的差异不显著(P0.05)。因此,在罗非鱼饲料中添加0.5%~1.5%的叶下珠可明显抑制罗非鱼肝损伤,增强罗非鱼的免疫性能。     

垂盆草提取物干预罗非鱼脂肪性肝病作用机制的代谢组学研究

为探究垂盆草提取物对吉富罗非鱼(Oreochromis niloticus)脂肪性肝病的干预作用及机制, 实验配制对照组 (0%大豆油, 0%垂盆草提取物)、高脂组(4%大豆油, 0%垂盆草提取物)和垂盆草干预组(4%大豆油, 0.12%垂盆草提取物) 3 种等氮饲料, 饲养初始体重为(11.63±0.66) g 的吉富罗非鱼 8 周后, 取吉富罗非鱼血清和肝脏, 采用非靶向代谢组学检测方法, 并结合肝脏组织透射电镜观察、血清生化指标结果进行分析。结果显示, 高脂组体重、增重率 (WGR)和特定生长率(SGR)显著低于对照组与垂盆草干预组(P＜0.05), 肝体比(HSI)、饲料系数(FRC)显著高于对照组与垂盆草干预组(P＜0.05)。透射电镜观察发现高脂组与对照组相比, 肝组织细胞超微结构异常, 垂盆草干预组与高脂组对比有所改善。血清生化指标显示垂盆草干预组较高脂组谷丙转氨酶(ALT)、谷草转氨酶(AST)、甘油三酯 (TG)、总胆固醇(T-CHO)、低密度脂蛋白胆固醇(LDL-C)、肿瘤坏死因子 α (TNF-α)和白细胞介素 8 (IL-8)水平显著降低(P＜0.05), 高密度脂蛋白胆固醇(HDL-C)、超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)和白细胞介素 10 (IL-10) 水平显著升高(P＜0.05)。肝脏代谢组学检测结果表明, 与对照组相比, 高脂组有 27 个差异代谢产物(DM), 富集到 19 条通路, 主要代谢通路为糖酵解/糖异生、丙酮酸代谢、β-丙氨酸代谢; 与高脂组相比, 垂盆草干预组有 23 个差异代谢产物, 富集到 9 条代谢途径, 主要代谢通路为 β-丙氨酸代谢和亚油酸代谢。上述结果表明, 垂盆草提取物对于干预吉富罗非鱼因高脂饮食引起的脂肪性肝病有积极作用, 其作用通路与 β-丙氨酸代谢、亚油酸代谢相关。     

Analysis of Streptococcus agalactiae‐induced liver injury in tilapia (Oreochromis niloticus)

Streptococcosis, a bacterial disease for multiple fish species, especially tilapia, caused more disruption to the fish culture industry. However, the underlying mechanisms for the occurrence of streptococcosis remain unclear. The aim of this study was to study the effects of streptococcus on the liver of tilapia. In this study, tilapia were injected streptococcal solution (0.05 ml/10 g body weight) and collected blood and liver at 4, 8, 24, 48, 72, 96, 120 and 144 hr after injection. The results showed that the activities of glutamate oxalate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (AKP) and superoxide dismutase (SOD) in the serum of tilapia exhibited irregular changes: increase at first, then decrease and increase again. The levels of total antioxidant capacity (T‐AOC), glutathione (GSH) and malondialdehyde (MDA) showed a decreasing tendency in serum after injection, except GSH at 4 hr. The activity of catalase (CAT) decreased in serum at 4, 24, 120 and 144 hr after injection of streptococcal solution, while the content TP enhanced in serum at 48, 72 and 120 hr after injection. Observations of pathological sections showed obvious damage to the liver tissue structure in response to streptococcal infection. Western blotting revealed an increase in ikkbeta (Ikkβ) protein with prolonged infection time and a decrease in NF‐kappa‐B inhibitor alpha (IkB‐α) and ikappab kinase alpha (Ikkα) proteins. The gene expression of cytochrome P4501A (CYP1A) was downregulated in liver at 24 and 48 after injection, while the mRNA levels of heat stress protein 70 (HSP70) and tumour necrosis factor alpha (TNF‐α) increased at 48 and/or 72 hr. Taken together, our findings confirmed that streptococcus can cause serious damage to the liver of tilapia.     

Buprofezin toxication implicates health hazards in Nile tilapia (Oreochromis niloticus)

The objective of this study was to investigate the toxic effects of buprofezin insecticide on Nile tilapia (Oreochromis niloticus). The fish were exposed to buprofezin at 100 mg/L for 28 days. Compared to control, activity of serum transferases and levels of urea and creatinine showed significant increases. Oxidative stress was recorded manifested by elevated levels of malondialdehyde (MDA), reduced concentrations of reduced glutathione (GSH) and inhibition of activities of superoxide dismutase (SOD) and catalase (CAT) in liver and kidney. Examination of peripheral RBCs revealed elevated frequency of micronucleated cell. Interleukin 1 beta (IL‐1β) gene was upregulated in liver, muscle and brain, while that of cyclooxygenase 2 (COX‐2) gene increased in liver and muscle, but not in brain. Histopathological alterations were recorded in liver, kidneys, brain, gills, pancreas, spleen, intestine, muscle and ovaries. The immunohistochemical detection of caspase‐3 in the liver revealed no differences between treated and control groups; however, the expression of inducible nitric oxide synthase (iNOS) was demonstrated in hepatocytes and hepatopancreas in buprofezin‐treated group compared to control. It has been concluded that the tissue damage induced by buprofezin in Nile tilapia is mediated by oxidative stress and inflammatory response but not by apoptosis.     

Influence of Stocking Density on Growth Performance,Antioxidant Status,and Physiological Response of Juvenile Turbot,Scophthalmus maximu,Reared in Land‐based Recirculating Aquaculture System

This study aimed to assess the effects of stocking density on the growth, antioxidant status, and physiological response of juvenile turbot. Turbot (average initial weight 70.0 ± 5 g) were reared at three different initial densities (low density [LD], 5.13 ± 0.03 kg/m²; medium density [MD], 7.71 ± 0.11 kg/m²; and high density [HD], 10.8 ± 0.12 kg/m²) for 80 d. At the end of this trial, the final densities were 13.2 ± 0.10, 19.9 ± 0.15, and 25.7 ± 0.12 kg/m² in the LD, MD, and HD groups, respectively. The growth performances were adversely influenced by a high stocking density. Levels of cortisol, glucose, cholesterol, triglyceride, glutamate pyruvate transaminase, and glutamate oxalate transaminase in the plasma significantly increased in HD treatment. Results of oxidative stress analyses showed that there was a clear decrease in superoxide dismutase, glutathione peroxidase, catalase, glutathione, and total antioxidant capacity, and an obvious increase in malondialdehyde in plasma and/or liver of turbot reared in HD group (P < 0.05). Overall, the results indicated that increasing stocking density reduced the growth performance, modulated the physiological response, and induced oxidative stress in turbot.     

怀山药皮对淇河鲫血清生化、免疫指标及组织结构的影响

为探究怀山药皮(Chinese yam peel,YP)对淇河鲫免疫的影响,选取平均体重为(106.76±3.74)g的淇河鲫240尾,随机分为对照组(NC)、0.5%怀山药皮添加组(LYP)、1%怀山药皮添加组(MYP)、2%怀山药皮添加组(HYP)4组,养殖8周,检测实验鱼生长指标、血清生化指标及免疫相关基因的表达情况。结果显示:添加怀山药皮对淇河鲫生长指标没有显著性影响;血液生化指标中谷草转氨酶活性在MYP组显著性降低,碱性磷酸酶的活性显著升高;与NC组相比,怀山药皮添加组肝脏细胞膜与核膜完整性增强,胞质破碎,核溶解、偏移现象减轻;与NC组相比,添加怀山药皮上调了抑炎因子(IL-10)、紧密连接蛋白基因(Claudin-1)、抗氧化基因(CAT和GST)和TLR通路基因(TLR4)mRNA表达量。以上结果表明,饲料中添加怀山药皮,能在一定程度上增强鱼体免疫力。     

白藜芦醇对脂多糖诱导草鱼肾脏细胞炎症的抑制作用

为评价白藜芦醇(resveratrol)对脂多糖诱导损伤草鱼(Ctenopharyngodon idella)肾脏细胞(CIK)的保护作用,本研究通过脂多糖(LPS)诱导细胞炎症损伤,测定和分析白藜芦醇对CIK细胞抗氧化因子活性和抗氧化、炎症相关基因表达变化的影响。结果表明,与对照组相比,LPS处理导致CIK细胞活力降低(P<0.05),乳酸脱氢酶(LDH)活性升高(P<0.05),降低了细胞内过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的活性,并导致还原型谷胱甘肽(GSH)浓度降低(P<0.05)和丙二醛(MDA)含量升高(P<0.05)。此外,LPS处理能引起CIK细胞的CAT、TNF-α、IFN-γ、IL-1基因表达显著上调(P<0.05),而对IL-10和SOD基因的转录表达无显著影响(P>0.05)。通过向培养基中添加白藜芦醇(4μg/mL)可以显著减弱LPS对CIK细胞造成的损伤,维系细胞抗氧化能力,抑制TNF-α等炎症相关基因的表达(P<0.05),促进CAT基因的表达(P<0.05)。研究认为白藜芦醇对LPS造成的CIK细胞损伤有明显的干预作用,主要原因可能是由于白藜芦醇对CIK细胞的抗氧化能力的改善以及对促炎因子表达的抑制。本研究可为白藜芦醇应用于鱼类炎症、氧化损伤相关疾病的防治提供理论依据。     

Effects of ferulic acid on growth performance,immunity and antioxidant status in genetically improved farmed tilapia (Oreochromis niloticus) fed oxidized fish oil

A study was conducted to characterize the effects of dietary oxidized fish oil on the growth performance, immunity and antioxidant status of genetically improved farmed tilapia (Oreochromis niloticus) and to determine the role of ferulic acid on the oxidative damage induced by the oxidized fish oil. The tilapia (13.73 ± 0.31 g) were fed four experimental diets containing untreated (peroxide value, POV: 2.2 meq/kg) and highly oxidized (POV: 120.6 meq/kg) fish oil either with or without ferulic acid (0 or 400 mg/kg) supplementation for 12 weeks. From the results, the oxidized fish oil treatments increased antioxidant enzyme activities and MDA values but decreased the weight gain and the immunological parameters in tilapia. Meanwhile, the serum biochemical indices were significantly affected by the oxidized fish oil. Besides, the addition of ferulic acid partially counteracted the free radical‐induced damage and improved the health status of tilapia. In conclusion, the oxidized fish oil may induce oxidative stress, destroy liver, dysregulate lipid metabolism as well as reduce non‐specific immunity, and eventually result in growth inhibition of tilapia. The ferulic acid supplementation partially offset the negative effects of the oxidized fish oil on tilapia.     

Tissue-specific responses of oxidative stress biomarkers and antioxidant defenses in rainbow trout Oncorhynchus mykiss during a vaccination against furunculosis

The present study was conducted to evaluate the effects of vaccination against furunculosis on responses of oxidative stress and antioxidant defenses in rainbow trout Oncorhynchus mykiss muscle, gills, liver, and brain tissues. The oxidative stress markers (malondialdehyde and carbonyl derivatives of protein oxidative destruction levels), antioxidant defenses (superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase), and total antioxidant capacity in different tissues of rainbow trout were measured. Our data showed that exposure of trout to vaccine against furunculosis produced changes (either increase or decrease) in oxidative stress and antioxidant enzymes responses, and these responses showed marked organ differences, associated with tissue patterns. Our study demonstrated that vaccinated trout showed alteration in antioxidant defenses and oxidative stress responses, with higher severity in the liver, compared with other tissues. Our data also suggest that vaccination against furunculosis induced lipid peroxidation in gill and liver tissues. However, muscle and brain tissue are capable of restoring its pro- and antioxidant balance after vaccination.     

Effects of α‐lipoic acid on growth performance,body composition,antioxidant profile and lipid metabolism of the GIFT tilapia (Oreochromis niloticus) fed high‐fat diets

The wide use of lipid as a non‐protein energy substitute has led to lipid metabolic problems in cultured tilapia. Therefore, studies that reduce the effects of high‐fat diets in genetically improved farmed tilapia (GIFT) are required. This study evaluated the optimum level and effects of dietary α‐lipoic acid (α‐LA) on growth performance, body composition, antioxidant capacity and lipid metabolism of GIFT tilapia. The basal diet (120 g/kg lipid) was supplemented with six concentrations of α‐LA at 0 (control), L300, L600, L900, L1200 and L2400 mg/kg diet to make the experimental diets, which were fed to GIFT tilapia juveniles (initial body weight: 0.48 ± 0.01 g) for 8 weeks. The weight gain of fish improved significantly in the L300 than other dietary treatments. The intraperitoneal fat index and lipid content of fish fed on the L2400 diet decreased significantly than those fed on the control diet. The activities of superoxide dismutase and glutathione peroxidase (GSH‐Px) in serum and liver were significantly higher in fish fed on the L300 diet than the control. The reduced GSH content of fish fed on the L300 in serum and liver was significantly higher than those fed on control diet. The malondialdehyde content in serum and liver was significantly lower in L300 than in the control. The adipose triglyceride lipase gene was significantly up‐regulated in fish fed on the L2400, but the diacylglycerol acyltransferase 2 gene was down‐regulated in adipose. The liver‐type fatty acid‐binding protein gene in the liver was significantly up‐regulated in fish fed on the L300 and L600 diets. Moreover, the acyl‐coenzyme A oxidase gene in liver was significantly up‐regulated in fish fed on the L300, L600, L900 and L1200 diets. Polynomial regression analysis indicated that 439–528 mg/kg α‐LA is an appropriate dosage in high‐fat diet to improve growth performance and relieve lipid oxidative damage by accelerating lipid catabolism and reducing lipid synthesis in GIFT tilapia.     

Lead (Pb) accumulation,oxidative stress and DNA damage induced by dietary Pb in tilapia (Oreochromis niloticus)

With the increasing occurrence of dietary lead (Pb) contamination in aquaculture, a better understanding of the toxic effects of dietary Pb on aquatic animals is needed. Tilapia (Oreochromis niloticus) were exposed to dietary Pb at concentrations of 0, 100, 400 and 800 μg g^?1 dry weight for 60 days, and Pb accumulation in tissues and blood, oxidative stress in posterior kidney and DNA damage in peripheral blood cells were investigated. The results showed that dietary Pb exposure resulted in significant Pb accumulation in tissues and blood, which increased with the dietary Pb concentrations. Pb accumulated in sampled tissues in the following order: posterior kidney>bone>liver>gill>spleen>testis>muscle>brain. Dietary Pb caused a significant increase in the malondialdehyde level and a significant decrease in the total antioxidant capacity content when compared with the control group (P<0.05), accompanied by concentration‐dependent decreases in the glutathione content, glutathione peroxidase and superoxide dismutase activities. Pb dose‐dependent DNA damage was observed in peripheral blood cells of tilapia exposed to dietary Pb. The results suggest that dietary Pb exposure can induce significant Pb accumulation in tissues and blood, followed by oxidative stress in posterior kidney and DNA damage in peripheral blood cells of tilapia.     

Amelioration of LPS‐induced inflammatory response and oxidative stress by astaxanthin in Channa argus lymphocyte via activating glucocorticoid receptor signalling pathways

The present study was conducted to evaluate the effects of astaxanthin (AST) against lipopolysaccharide (LPS)‐induced lymphocyte viability, ultrastructural lesions, apoptosis, oxidative stress and inflammatory responses in Channa argus. Lymphocytes exposed to more than 10 μg/ml LPS alone for 24 hr showed significantly decreased cell viability, elevated nitric oxide (NO) and malondialdehyde (MDA), lactate dehydrogenase (LDH) contents, and increased nuclear factor κB p65 (NF‐κB p65), myeloid differential protein‐88 (MyD88), tumour necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), interleukin‐8 (IL‐8), caspase‐3, caspase‐8 and caspase‐9 gene expression. LPS at a concentration of 10 μg/ml could induce oxidative stress and inflammatory responses in lymphocytes. The activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD)) were significantly decreased after exposure to 10 μg/ml LPS. Besides, AST strikingly antagonized the LPS‐induced negative effects. AST significantly increased the expression of HSP70, HSP90, IκB‐α, and glucocorticoid receptor (GR) and decreased inflammatory responses. Further study showed that AST can activate GR signalling pathway and inhibit p65 phosphorylation. In addition, AST attenuated LPS‐induced apoptosis, mitochondrial swelling, degeneration and vacuolization. Collectively, these findings suggest that AST has protective roles in LPS‐induced cell damage via modulating GR activation in C. argus lymphocytes.