| 镉对罗非鱼鳃线粒体结构和能量代谢的影响 |
| 摘要点击 1361 全文点击 1384 投稿时间：2006-02-17 修订日期：2006-03-28 |
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| 中文关键词 镉 罗非鱼 鳃 氧化损伤 能量代谢 |
| 英文关键词 cadmium Oreochromis niloticus gill oxidative damage energy metabolism |
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| 中文摘要 |
| 为探明水环境镉对罗非鱼(Oreochromis niloticus)鳃线粒体结构和能量代谢的影响及其作用机理，本研究采用室内模拟方法，将罗非鱼在Cd2+浓度为0 μg/L、50 μg/L和500 μg/L的水中暴露7 d后，观察鳃线粒体超微结构并测定线粒体超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和鳃组织中磷酸果糖激酶(PFK)、ATP酶(ATPase)活性、乳酸(LD)、ATP、ADP、AMP含量及血浆中Na+、K+、Ca2+浓度和渗透压，并计算能荷值(EC).结果表明，50 μg/L组鱼鳃线粒体结构未受损， 除SOD酶活性被显著诱导外,其余测定指标与对照组相比无显著差异(p>0.05); 而500 μg/L组鱼鳃线粒体严重受损， LD、MDA、ADP、AMP和血浆K+含量显著高于对照组， SOD和ATPase活性显著低于对照组(p<0.05)， PFK和渗透压无显著变化(p>0.05),但有降低趋势.结果表明,高浓度镉短期暴露将降低鱼鳃线粒体SOD活性而导致线粒体氧化损伤,同时抑制ATPase和PFK活性,影响鳃的能量供应和利用，最终降低鳃血浆渗透压和离子浓度调节能力可能是其毒性机理之一. |
| 英文摘要 |
| To explore the effects of waterborne cadmium (Cd) on the mitochondrion structure and cellular energy metabolism in gills of tilapia (Oreochromis niloticus) and possible mechanisms,specimens of tilapias were exposed to different Cd2+ concentrations (0,50,500 μg/L freshwater) for 7 days under indoor simulate condition. At the end of the experiment,ultrastructure and superoxide dismutase (SOD) activity as well as malondialdehyde (MDA) level of branchial mitochondria were detected,while the phosphofructokinase (PFK) and ATPase activities and the contents of lactic acid (LD)，ATP,ADP,AMP in gill tissues and osmolality,Na+,K+ and Ca2+ concentrations in plasma were assayed,and the energy charge (EC) was also calculated. The results showed that the structure of mitochondria in fish exposed to 50 μg/L Cd2+ was intact and there were no significant differences except the significant elevation in SOD activity in all biochemical indicators examined as compared to the control (p>0.05). However,in fish exposed to 500 μg/L Cd2+,mitochondria were damaged severely,SOD and ATPase activities were decreased significantly whereas the contents of LD,MDA,ADP and AMP as well as concentration of K+ in plasma in comparison with the control values were enhanced significantly (p<0.05),in addition,there was a decreasing trend in PFK activity and plasma osmolality though the difference was not significant (p>0.05). The present findings suggested that the short-term exposure to higher concentrations of Cd2+ would lead to the obstruction of energy supply and utilization due to inhibited ATPase and PFK activity as well as oxidative damage to mitochondria resulting from decreased SOD activity,and decrease the ability of gills to regulate the plasma ion composition and osmolality,which would be one of the possible mechanisms for Cd2+ toxicity. |
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