摘要
目的通过观察甲醛吸入对大鼠肾组织中超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、过氧化氢酶(CAT)和脂质过氧化物(MDA)水平的影响,探讨其对肾组织氧化损伤的作用机制。方法用不同剂量的气态甲醛对大鼠进行染毒;用相应的试剂盒对组织中SOD、CAT的活性和GSH、MDA的含量进行测定。结果吸入1.0 mg/m3甲醛时,肾组织中MDA含量与对照相比明显升高,其值为(0.41±0.02)nmol/mg pro(P<0.001);吸入0.5 mg/m3甲醛,即可引起GSH含量降为(1.12±0.97)mg/mg pro(P<0.05)。但甲醛吸入时,SOD和CAT的活性无明显改变(P>0.05)。结论甲醛可抑制肾组织的抗氧化能力,引发脂质过氧化,造成肾组织的氧化损伤。
Objective To investigate the superoxide dismutase （SOD） and catalase （CAT） activities as well as the glutathione （GSH） and malondialdehyde （MDA） levels in renal tissue after inhalation exposure to formaldehyde （ FA） , and the mechanism of oxidation damage caused by FA. Methods The rats were exposed to different concentrations of gaseous HCHO 8 hours per day for six weeks. SOD and CAT activities, GSH and MDA levels were measured by their reagent boxes respectively. Results Inhalation exposure to 1.0 mg/m^3 FA,MDA levels in renal tissue increased to （0. 41 ±0. 02 ） nmol/mg pro in comparison with the control （ P 〈0. 001 ）. GSH levels decreased to （1.12 ±0. 97） mg/mg pro in rats exposure to 0. 5 mg/m±3 HCHO （P 〈0. 05）. No statistically considerable differences were found in SOD and CAT activities （P 〉0. 05）. Conclusion The toxic effect of inhaled FA appears to inhibit the capability of anti-oxidation system in renal tissue, and leads to lipid peroxidation. In conclusion,FA can induce oxidation damage in rats＇renal tissue.
出处
《滨州医学院学报》
2008年第6期409-410,414,共3页
Journal of Binzhou Medical University
基金
滨州医学院科技计划(BY2006KJ27)
