摘要
目的研究急性汞中毒与氧化应激反应之间的关系,并探讨其机制。方法皮下注射1%氯化高汞(HgCl_2,1.7 ml/kg)溶液,导致家兔急性中毒。动态观察血尿素氮(BUN)、血浆丙二醛(MDA)含量和血浆铜蓝蛋白(CP)、乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)及红细胞超氧化物歧化酶(SOD)活力的变化;检测肾皮质、肺、肝、心及脾脏组织匀浆MDA含量和SOD的活力;同时检测尿蛋白和尿沉渣。结果注射HgCl_2后10 h和24 h尿中出现大量的蛋白和管型;血浆BUN和MDA含量及CP、LDH和ACP活力明显高于注射HgCl_2前和对照组;红细胞SOD活力明显低于注射HgCl_2前和对照组(P<0.05或P<0.01),且随汞中毒时间延长而更加明显。结论急性汞中毒的发生与氧化应激反应有关。注射HgCl_2后,体内氧化应激反应加强,氧化程度超出氧化物的清除,使促氧化与抗氧化系统平衡失调,进而导致全身的脂质过氧化损伤。
Objective To study the relation between acute mercury poisoning and oxidative stress and their mechanism.Methods Models of acute mercury poisoning were made in rabbits.The content of urea nitrogen(BUN) in blood,malondialdehyde(MDA) and the activity of copper—protein(CP),lactate dehydrogenase(LDH) and acid phosphatase(ACP) in plasma were measured,superoxide dismutase(SOD) in erythrocyte,and MDA and SOD in tissues homogenate were observed.Results It showed that BUN,CP, MDA,LDH and ACP increased,and SOD reduction after mercury poisoning,compared with the control group and before mercury injection,the difference was statistical significant(P〈0.05 or P〈0.01). Conclusions It suggests that acute mercury poisoning may result in the increase of oxidative stress,and the anti—oxidative ability in the body becomes gradually decreased.The development of acute mercury poisoning is closely related to the change of oxidative stress and the anti—oxidative ability.
出处
《工业卫生与职业病》
CAS
CSCD
北大核心
2010年第4期230-233,共4页
Industrial Health and Occupational Diseases
基金
华北煤炭医学院科研基金资助(3099)
关键词
汞中毒
氧化应激
脂质过氧化
丙二醛
超氧化物歧化酶
Mercury poisoning
Oxidative stress
Lipid-peroxidation
Malondialdehyde
Superoxide dismutase