亚硝酸盐急性中毒小鼠肝损伤机理探讨

Study on Mechanism of Acute Poisoning and Hepatic Injury Induced by Sodium Nitrite in Mice

目的:研究探讨亚硝酸盐急性中毒小鼠肝损伤作用及机理。方法:将小鼠随机分为正常对照组、亚硝酸盐低、中、高剂量组。采用分光光度法测定小鼠肝组织的丙二醛(MDA)、谷光甘肽(GSH)的含量以及谷丙转氨酶(ALT)的活性;采用聚丙烯酰胺凝胶电泳(PAGE)检测超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)的活性。结果:与正常对照组比较,亚硝酸盐各组小鼠肝脏MDA含量明显增高,以中、高剂量组差异显著(p<0.05和p<0.01);转氨酶ALT活性均明显降低(p<0.01),GSH含量均有所增高,以低剂量组差异显著(p<0.01),结果呈现随亚硝酸盐剂量增加MDA含量增高、ALT活性及GSH含量下降的趋势。同时SOD、LDH的同工酶电泳结果显示,SOD和LDH的酶活随着亚硝酸盐剂量增高而明显下降。结论:亚硝酸盐急性中毒,可导致小鼠肝组织受损,其损伤程度随剂量增加而加重,损伤机理与肝脏严重缺氧和自由基增多有关。

In this study, the mice were divided into four groups （normal group, low-dosage group of sodium nitrite, middledosage group of sodium nitrite and high-dosage group of sodium nitrite）. Spectrophotometric method was used to detect the contents of maleic dialdehyde （MDA） and glutathione （GSH） and the activity of alanine aminotransferase （ALT） in the liver. Lactate dehydrogenase （LDH） and superoxide dismutase （SOD） isoenzyme in the liver were determined by polyacrylamide gel electrophoresis （PAGE）. The results showed that by compared with the control group, the MDA level of sodium nitrite groups is increased remarkably, the activity of ALT in sodium nitrite groups is decreased obviously （p 〈 0.01）, and the GSH content is enhanced in sodium nitrite groups, especially in low-dosage group （p 〈 0.01）. Meanwhile isoenzyme electrophoresis indicated that the activities of LDH and SOD are reduced following with the increase of sodium nitrite dosage. In conclusion, the hepatic tissue is damaged by acute poisoning with nitrites, and the degree of injury is aggravated following with the increase of nitrites content. The mechanism of hepatic injury may be connected with severe hypoxia and the increase of free radicals in liver.