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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 relationship between acute mercury poisoning and oxidative stress and to explore its mechanism. Methods Subcutaneous injection of 1% HgCl 2, 1.7 ml / kg solution resulted in acute poisoning in rabbits. The levels of blood urea nitrogen (BUN), plasma malondialdehyde (MDA) and plasma ceruloplasmin (CP), lactate dehydrogenase (LDH), acid phosphatase (ACP) and erythrocyte superoxide dismutase (SOD) Vitality changes; detection of renal cortex, lung, liver, heart and spleen homogenate MDA content and SOD activity; simultaneous detection of urinary protein and urinary sediment. Results A large amount of protein and tube appeared in urine at 10 h and 24 h after injection of HgCl 2. The content of BUN and MDA, the activity of CP, LDH and ACP in plasma of HgCl 2 injection group were significantly higher than those of HgCl 2 injection group and control group. The activity of SOD in erythrocytes was significantly lower than that before injection of HgCl 2 And control group (P <0.05 or P <0.01), and with mercury poisoning time is more obvious. Conclusion The occurrence of acute mercury poisoning is related to oxidative stress. After injection of HgCl 2, the in vivo oxidative stress response is strengthened, the degree of oxidation is beyond that of oxide, so that the balance of pro-oxidant and anti-oxidant systems is out of balance, which leads to the systemic lipid peroxidation injury.