Lu Zhong-Qiu, Qiu Qiao-Meng, Miao Xin-Jun, Hu Guo-Xin
Department of Emergency, The First Affiliated Hospital, Wenzhou Medical College, Wenzhou, Zhejiang, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2007 Apr;19(4):233-5.
To study the change in oxidase and anti-oxidase in liver of the mice poisoned by dimethylformamide (DMF), and the effects of the treatment with sulfhydryl compounds in acute poisoning of DMF.
The sulfhydryl compounds included sodium dimercaptopropane (Na-DMPS), N-acetylcysteine (NAC), glutathione (GSH) and dimercaptosuccinic acid (DMSA). The model of acute poisoning with DMF in mice was reproduced, and the left hepatic lobes were harvested at 6, 12, 24, 48 and 72 hours after DMF to detect the dynamic changes in the activities of superoxide dismutase (SOD) and xanthine oxidase (XOD) in liver homogenate. Treatment groups included intraperitoneal injection of Na-DMPS, NAC, GSH, DMSA respectively. In the control groups, the activities of XOD and SOD in liver were determined 24 hours after intragastric administration of DMF.
The activities of XOD, SOD in liver were elevated at 24 hours after intragastric administration of DMF (both P<0.01), and returned to the normal levels at 48-72 hours. Compared to the poisoning group, the activities of XOD, SOD in liver homogenate were significantly lowered after the treatment of Na-DMPS, NAC and DMSA (P<0.05 or P<0.01). The activity of XOD in liver homogenate was reduced 24 hours after treating with GSH (P<0.05), and no obvious change was observed in SOD (P>0.05). As far as the activity of SOD was concentrated, Na-DMPS, NAC, DMSA showed better effects than GSH (all P<0.05), and Na-DMPS was the best. There was no significant differences in XOD among the four sulfhydryl compounds.
The balance of oxidase and anti-oxidase is interrupted by DMF, which might be one of the mechanisms of damage to the liver. Na-DMPS, NAC and DMSA could protect liver function by restoring the balance.
研究二甲基甲酰胺（DMF）中毒小鼠肝脏氧化酶和抗氧化酶的变化，以及巯基化合物对DMF急性中毒的治疗作用。
巯基化合物包括二巯丙磺酸钠（Na-DMPS）、N-乙酰半胱氨酸（NAC）、谷胱甘肽（GSH）和二巯基丁二酸（DMSA）。复制小鼠DMF急性中毒模型，于DMF染毒后6、12、24、48和72小时摘取左肝叶，检测肝匀浆中超氧化物歧化酶（SOD）和黄嘌呤氧化酶（XOD）活性的动态变化。治疗组分别腹腔注射Na-DMPS、NAC、GSH、DMSA。对照组于灌胃DMF 24小时后测定肝脏XOD和SOD活性。
灌胃DMF 24小时后肝脏XOD、SOD活性升高（均P<0.01），48~72小时恢复正常水平。与中毒组比较，Na-DMPS、NAC和DMSA治疗后肝匀浆XOD、SOD活性显著降低（P<0.05或P<0.01）。GSH治疗24小时后肝匀浆XOD活性降低（P<0.05），SOD无明显变化（P>0.05）。就SOD活性而言，Na-DMPS、NAC、DMSA效果优于GSH（均P<0.05），其中Na-DMPS最佳。4种巯基化合物XOD活性差异无统计学意义。
DMF破坏氧化酶与抗氧化酶的平衡，可能是肝脏损伤机制之一。Na-DMPS、NAC和DMSA可通过恢复平衡保护肝功能。
