丙二醛对离体草鱼肠道黏膜细胞的损伤作用

以丙二醛为实验材料, 在草鱼Ctenopharyngodon idella肠道黏膜细胞培养液中加入不同浓度丙二醛, 研究丙二醛不同剂量、不同作用时间下对肠道黏膜细胞生长、细胞形态结构及相关酶活性的变化. 结果显示: 添加(1.23-9.89) mol/L丙二醛在3-9h时显著抑制了离体草鱼肠道黏膜细胞生长及存活率, 以6h时抑制程度较为明显, 导致贴壁细胞减少, 细胞集落面积减小, 其中添加4.94 mol/L丙二醛细胞胞浆内脂肪滴沉积, 空泡变性, 同时线粒体肿胀, 核固缩; 丙二醛对细胞分化成熟有抑制, 且增加细胞器膜的通透性, 导致胞浆酶漏出; 6h时丙二醛处理组培养液中GSH-PX、T-AOC活力显著降低(P0.05). 结果表明: 添加(1.23-9.89) mol/L丙二醛对草鱼肠道黏膜细胞产生了损伤, 表现为抑制细胞生长, 改变细胞形态、结构, 导致膜结构破坏, 且作用程度与添加浓度、作用时间呈正相关关系. 研究认为丙二醛对草鱼肠道黏膜细胞具有显著性的损伤作用.  

Damage of MDA on intestinal epithelial cells in vitro of grass carp (Ctenopharyngodon idella)

The present study investigated the deleterious effects of MDA on the growth, morphology, structure and related enzyme activity of intestinal epithelial cells (in vitro) isolated from Ctenopharyngodon idella. MDA reduced cell activity. Cell survival at the range of 1.23-9.89 g/L for 3-9h treatments; the highest inhibition was at 6 hour. MDA also reduced cell adhesion and colony formation. With the concentration of 4.94 g/L MDA induced the formation of fat droplets and vesicles, swelling mitochondria, and karyopycnosis. MDA inhibited cell differentiation, induced intracellular enzyme leakage, and increased organelles membrane permeability. MDA significantly reduced the activity of GSH-PX and T-AOC in culture medium (P0.05). In conclusion, MDA at the concentration range of 1.23-9.89 g/L damaged the dissociated IECs from Ctenopharyngodon idella by disregulating cell growth, cell morphology, cell structure, and lipid peroxidation. The extent of damage is correlated with the concentration and incubation time.