摘要
目的探讨不同剂量的右旋糖酐铁对小鼠肝脏抗氧化水平和病理损伤的影响。方法将雌雄各半的昆明小鼠随机分为4组,以不同浓度的右旋糖酐铁隔日腹腔注射(IP),注射6周后,测定肝组织中丙二醛(MDA)的含量、超氧化物歧化酶(SOD)以及谷胱甘肽过氧化物酶(GSH-PX)的活性,测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)、酸性磷酸酶(ACP)活性,并做肝脏病理组织学检查。结果与正常对照组相比,肝组织中MDA的含量较对照组明显升高(P<0.001),SOD和GSH-PX的活性则明显下降(P<0.001)。血清ALT、AST活性较对照组明显升高(P<0.001),且有剂量效应关系;而血清AKP、ACP活性较对照组则无显著性差异(P>0.05)。病理组织学检查,经铁染色后镜下可见低剂量组有少量铁均匀分布,中高剂量组则有大量铁存在。结论过量的铁可对肝脏造成严重的损害,且呈剂量依赖性,其机制可能与铁在肝脏内代谢释放出铁离子,游离的铁离子介导脂质过氧化而造成肝脏损害有关。
Objective To study the level of mice liver antioxygen and the degree of mice fiver pathologiccal damage through intraperitoneal injection of different dose of iron dextran in mice. Method Male and female mice were randomly divided into four groups and were ntraperitoneally injected with different doses of iron dextran every the other day, for six weeks. The levels of MDA, SOD and GSH-PX in the liver and the levels of ALT, AST, AKP and ACP in the blood-serums were measured. Pathohistology analysis of the liver was also performed. Result Comparing with the normal group, the MDA level in the liver was significantly increased （P〈0.001）, and the levels of SOD and GSH-PX were dramatically decreased （P〈 0.001 ）. There is no significant difference the levels of AKP and ACP between the normal group and the treated group. The pathohistology examination result showed that iron scatter in the low-dose treated group was more than that in the high-dose group. Conclusion Excess iron cause severe damage of the liver in a dose dependent manner. The mechanism may be the ferrous which release from liver cause lipid peroxidation.
出处
《热带医学杂志》
CAS
2007年第2期129-132,共4页
Journal of Tropical Medicine
关键词
铁
肝损伤
脂质过氧化
iron
liver damage
lipid peroxidation
