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为了探讨饲料氧化鱼油对草鱼(Ctenopharyngodon idellus)肠道组织结构及其通透性的影响,本实验以豆油、鱼油及氧化鱼油作为饲料脂肪源,分别设计鱼油组(6F)、豆油组(6S)、2%氧化鱼油(4S2OF)、4%氧化鱼油(2S4OF)及6%氧化鱼油(6OF)5组等氮、等能的半纯化饲料。经72d池塘网箱养殖后,实验结果显示:(1)氧化鱼油显著增加(P<0.05)草鱼血清和肠道MDA含量、增加肠道GSH含量(P<0.05),但随氧化产物含量上升GSH含量出现下降。(2)氧化鱼油会显著降低肠道内胆汁酸的含量(P<0.05)。(3)氧化鱼油会显著增加肠道绒毛中杯状细胞的数量(P<0.05),且随着氧化产物的增加,肠道微绒毛高度呈现先上升后下降趋势。(4)氧化鱼油会导致肠道紧密连接间隙增大,增加肠道通透性,使血清中D-乳酸及内毒素含量显著增加(P<0.05)。结果表明,饲料中鱼油氧化产物损伤了草鱼肠道组织结构,尤其是肠道上皮细胞紧密连接结构损伤严重,从而破坏了肠道黏膜的机械屏障功能,使肠道通透性显著增加,肠道细菌内毒素等发生转移。鱼油氧化产物会引起草鱼肠道氧化与抗氧化应激反应,干扰草鱼“肝-肠”正常胆汁酸循环,致使草鱼肠道胆汁酸不足。
In order to investigate the effect of feed oxidized fish oil on intestinal tissue structure and permeability of grass carp (Ctenopharyngodon idellus), soybean oil, fish oil and oxidized fish oil were used as feedstuff fat source to design fish oil group (6F), soybean oil group (6S) , 2% oxidized fish oil (4S2OF), 4% oxidized fish oil (2S4OF) and 6% oxidized fish oil (6OF) The results showed that: (1) Oxidized fish oil significantly increased MDA content in serum and gut (P <0.05) and increased GSH content in intestinal tract (P <0.05), but increased with the increase of oxidation product Content decreased. (2) Oxidation of fish oil significantly reduced intestinal bile acid content (P <0.05). (3) Oxidation of fish oil increased the number of goblet cells in intestinal villi significantly (P <0.05), and with the increase of oxidation products, the intestinal microvilli presented the trend of increasing firstly and then decreasing. (4) Oxidation of fish oil will lead to increased intestinal tight junction clearance, increase intestinal permeability, serum D-lactate and endotoxin levels increased significantly (P <0.05). The results showed that the fish oil oxidation products in the feed damaged the intestinal tissue structure of grass carp, especially the close connection structure of intestinal epithelial cells, which undermined the mechanical barrier function of intestinal mucosa and significantly increased the intestinal permeability, Bacterial endotoxin and other occurrence of transfer. Fish oil oxidation products can cause grass carp intestinal oxidation and antioxidant stress response, interfere with grass carp “liver - intestine ” normal bile acid cycle, resulting in grass carp intestinal bile acid deficiency.