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目的通过研究大鼠急性羰基镍中毒后血浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力的变化,探讨大鼠羰基镍急性毒性酶学作用及其中毒机制。方法SD大鼠静态吸入染毒30min,羰基镍染毒低、中、高剂量组浓度分别为20、135和250mg/m3,氯气染毒250mg/m3为阳性对照组。分别于染毒后第1、第2、第3和第7天测定血浆中SOD和GSH-Px活力。结果羰基镍中、高剂量组和氯气组SOD活力在第1、第2、第3天明显下降(P<0.05),第7天开始回升;羰基镍高剂量组SOD下降程度高于氯气组(P<0.05)。GSH-Px活力在羰基镍中、高剂量组染毒后第3天时出现下降(P<0.05)。结论羰基镍可明显抑制血浆中SOD和GSH-Px活力,使机体抗氧化能力下降,造成氧化损伤进而导致各种病变发生,并且该抑制作用以染毒后第1,第2,第3天最强。
Objective To study the changes of the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in plasma after acute nickel carbonyl poisoning in rats, mechanism. Methods SD rats were exposed to static inhalation for 30 minutes. The concentrations of carbonyl nickel in low, medium and high dose groups were 20, 135 and 250 mg / m3 respectively, and the chlorine exposure was 250 mg / m3 as the positive control group. Plasma SOD and GSH-Px activities were measured on the 1st, 2nd, 3rd, and 7th day after exposure respectively. Results The SOD activity in carbonyl nickel medium, high dose group and chlorine group decreased significantly (P <0.05) on the 1st, 2nd and 3rd days, and began to rise on the 7th day. The SOD level in the carbonyl nickel high dose group was higher than that in the chlorine group P <0.05). GSH-Px activity in carbonyl nickel, high-dose group on the 3rd day after treatment decreased (P <0.05). CONCLUSION Carbonyl nickel can obviously inhibit the activity of SOD and GSH-Px in plasma and decrease the antioxidative capacity of the body, leading to oxidative damage which leads to various pathological changes. The inhibitory effect of nickel carbonyl on the first, second and third days Strong.