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SOD是鱼类体内普遍存在的一种含有金属的酶，可以催化O2-•不均衡产生活性氧H2O2。这类活性氧又可使DNA断裂、脂质过氧化、酶蛋白失活等，从而引起机体氧化应激反应，在这些活性氧产生及转化中SOD等起着非常重要的作用。 在本研究中，斑马鱼暴露于L7-LPEAC中，体内的O2-•会增加，所以SOD为了歧化更多的O2-•，防止细胞膜系统过氧化作用的发生而被诱导，但是SOD产生的速度却跟不上机体内O2-•增加的速度，最终机体细胞膜系统过氧化。因此，SOD活性迅速下降。 斑马鱼肝脏中和鳃中SOD活性有所不同，可能是由于它们的生理功能不同造成。肝脏是解毒器官，鳃是呼吸器官。L7-LPEAC与鳃直接接触作用到很多靶组织细胞，短期内（如10 d），机体受L7-LPEAC胁迫而产生大量活性氧而无法耐受，为了清除多余的活性氧就要通过激活鳃中SOD等抗氧化酶类，从而使SOD活性明显升高，并且其活性随L7-LPEAC的质量浓度增大而增强。但当暴露时间的进一步延长，过高的L7-LPEAC会使鳃中的 H2O2不能及时清除而积累，使其中SOD活性受到抑制迅速下降。肝脏中SOD较为敏感，起初由L7-LPEAC引起的代谢紊乱产物透过鳃又汇集到肝脏，导致肝脏产生的过氧化物太多，超过了SOD消除的能力范围，使酶蛋白受损，肝脏SOD活性下降。此时鳃中SOD活性反相升高。随暴露时间的延长，鳃中SOD活性受到抑制迅速下降时，肝脏所承受的压力略有缓解而略微升高，但始终呈抑制状态。 |
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小老鼠1028(金币+17,VIP+0):很好，谢谢^_^ 9-12 11:59
小老鼠1028(金币+17,VIP+0):很好，谢谢^_^ 9-12 11:59
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不好意思啊，昨天有事耽误了。这是我翻的。你看看能用不？自己再修改一下。 SOD , existing commonly in fish ,is a kind of enzymes that contains metal .It can catalyze O2-• to reactive oxygen H2O2 unevenly. Such reactive oxygen can also enable DNA breakage, lipid peroxidation, enzyme inactivation, etc., causing oxidative stress response, in which process SOD plays a very important role. In this study,when the zebra fish exposed to L7-LPEAC, O2-• it contained will increase.Hence SOD is induced in order to disproportionate more O2-•to prevent the occurrence of the cell membrane system. However SOD's produced rate is not able to keep the increase speed of O2-• in the body.And eventually the body cell membrane peroxidation happened. As a result , SOD activity decreased rapidly. SOD activity is different in Zebra fish liver and gills ,due to their different physiological functions possibly. Liver is detoxification organs and gills are respiratory organs. L7-LPEAC acts to many target cells by contacting with the gills directly. In the short term (10 D, e.g.), the body producing plenty of reactive oxygen by the L7-LPEAC stress failed to tolerate . In order to remove the excess of reactive oxygen ,SOD and other antioxidant enzymes in gills are needed. Consequently ,SOD activity is significantly increased, and is enhanced with the increase of L7-LPEAC's mass concentration . But when the exposure time becomes longer, H2O2 in gills will be unable to clear in time and be accumulated because of excessive L7-LPEAC .Thus SOD activity declines rapidly. SOD in livers is more sensitive, Metabolic products initially caused by L7-LPEAC compiles to the liver through the gills, causing too much peroxide--exceeded the capacity of SOD to eliminate it. the enzyme protein is damaged,and SOD activity is decreased . At the same time SOD activity in gills RP-rises. With the time going , when the rapid decline of SOD activity in gills takes place ,the pressure on the liver is slightly increased ,but will still be inhibitory state. |
7楼2009-09-12 11:48:01
2楼2009-09-10 11:20:56
3楼2009-09-10 13:35:17
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SOD is a common practice in the body of fish contains a metal enzymes catalyze O2-• uneven generation of reactive oxygen H2O2. Such reactive oxygen species can also enable DNA breakage, lipid peroxidation, enzyme inactivation, etc., causing oxidative stress response, in which reactive oxygen species generation and transformation of SOD, etc. plays a very important role. In this study, the zebra fish exposed to L7-LPEAC, the body of O2-• will increase, so SOD in order to disproportionation more O2-•, to prevent the cell membrane system, the occurrence of peroxidation was induced, but the rate of SOD produced by has failed to keep the body O2-• the rate of increase and eventually the body cell membrane peroxidation. Thus, SOD activity decreased rapidly. Zebra fish liver and gills in the SOD activity in different may be due to a different cause of their physiological functions. The liver is the detoxification organs are the respiratory gills. L7-LPEAC the role of direct contact with the gills of many target cells, in the short term (eg, 10 d), the body by the L7-LPEAC stress arising from a large number of reactive oxygen species can not be tolerated, in order to remove the excess of reactive oxygen species through activation of gill should SOD and other antioxidant enzymes, so that SOD activity was significantly increased, and its activity with the L7-LPEAC the increase of mass concentration increased. But the further extension of exposure time, excessive L7-LPEAC gills of H2O2 will not be cleared in time accumulated, so that SOD activity which is inhibited to decline rapidly. SOD is more sensitive to the liver, initially from the L7-LPEAC metabolic disorder caused by the product of another pool to the liver through the gills, causing the liver to produce too much peroxide, more than the capacity of SOD to eliminate the scope of the enzyme protein damage, liver SOD decreased activity. At this point increase in gill SOD activity in RP. With the extension of exposure time, gill SOD activity was inhibited when the rapid decline in the liver by a slight easing the pressure slightly increased, but still showed inhibitory state. |
4楼2009-09-10 14:32:25