微囊藻毒素-LR对小鼠毒性机制的研究  

Toxicological Mechanisms of Microcystin-LR in Mice

作　　者：李哲[1] 边爱[1] 沈丽珍[1] 胥传来[1] 

机构地区：[1]江南大学食品学院,江苏无锡214122

出　　处：《食品科学》2010年第1期247-250,共4页Food Science

摘　　要：目的:探讨微囊藻毒素-LR(MC-LR)引起小鼠机体损伤可能的作用机制。方法:通过腹腔注射单次给予小鼠30μg/kgbw剂量的MC-LR,测定其在给药后1、4、8h的脏器系数和一些血液生化指标。结果:短时间内(给药后4h)肝脏系数显著增加,肾脏系数变化不明显;血液CAT含量显著上升,BUN先显著上升再显著下降;CAT活力显著上升;SOD变化不明显。结论:MC-LR首先攻击肝细胞,产生大量的自由基,破坏细胞膜,进而损伤了肝细胞,影响氨基酸的代谢,使肝脏充血、肿胀;接着又引发肾功能不全,使肾小管过滤能力降低;最后,随着时间的推移,对机体造成了潜在的永久伤害,但机体的修复功能使这种伤害表观上不可见,即MC-LR对机体造成的损害在一定程度上是可逆的。Objective：To explore the possible toxicological mechanisms of microcystin-LR（MC-LR） in mice.Methods：Organ index and blood biochemical parameters were examined in mice intraperioneally administered with microcystin-LR at the dose of 30 μg/kg bw at 1,4 and 8 h postadministration.Results：A significant increase in liver index of mice treated with MC-LR at 4 h postadministration was observed;but no obvious change in kidney index was observed at this time point.A significant increase in blood catalase（CAT） content and activity was determined.An initial increase and final decrease in blood urea nitrogen（BUN） was also monitored;however,superoxide dismutase（SOD） only exhibited little change.Conclusions：MC-LR attracts hepatocytes first,produces a large amount of free radicals,destroys cell membranes and heptocytes,interrupts metabolism of amino acids,and results in hyperemia and swelling of liver.Followed by liver damage,kidney insufficiency is also initiated;permeability of kidney tubules is increased as a result of MC-LR treatment.As the time goes on,MC-LR causes a permanent damage to organism.This damage,however,is not seen apparently due to repair function in the organism,that is,the MC-LRcaused damage to organism is reversible to a certain extent.

关 键 词：微囊藻毒素-LR 作用机制 脏器系数 血液生化指标 

分 类 号：TS201.6[轻工技术与工程—食品科学]