中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2014年
5期
376-377
,共2页
甲醛%超氧化物岐化酶%丙二醛
甲醛%超氧化物岐化酶%丙二醛
갑철%초양화물기화매%병이철
Formaldehyde%Superoxide dismutase%Malondialdchyde
目的 研究甲醛灌胃染毒对小鼠肝脏超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量的影响.方法 ICR小鼠30只,雌雄各半,随机分为3组,每组10只,雌雄各半,染毒剂量为:0、5、20 mg/kg体重,用灌胃的方法给予甲醛,每天1次,连续5d,对照组给予蒸馏水.取肝脏,用试剂盒测定各剂量组SOD活力和MDA含量.结果 与对照组比较,20 mg/kg染毒组小鼠肝脏中SOD活力明显降低,MDA的含量明显升高,差异有统计学意义(P<0.05),与对照组比较,20 mg/kg染毒组小鼠肝脏脏器系数明显升高,差异有统计学意义(P<0.05).结论 甲醛灌胃染毒对小鼠肝脏的脂质过氧化反应的平衡状态具有破坏作用,使其抗氧化能力明显降低.
目的 研究甲醛灌胃染毒對小鼠肝髒超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量的影響.方法 ICR小鼠30隻,雌雄各半,隨機分為3組,每組10隻,雌雄各半,染毒劑量為:0、5、20 mg/kg體重,用灌胃的方法給予甲醛,每天1次,連續5d,對照組給予蒸餾水.取肝髒,用試劑盒測定各劑量組SOD活力和MDA含量.結果 與對照組比較,20 mg/kg染毒組小鼠肝髒中SOD活力明顯降低,MDA的含量明顯升高,差異有統計學意義(P<0.05),與對照組比較,20 mg/kg染毒組小鼠肝髒髒器繫數明顯升高,差異有統計學意義(P<0.05).結論 甲醛灌胃染毒對小鼠肝髒的脂質過氧化反應的平衡狀態具有破壞作用,使其抗氧化能力明顯降低.
목적 연구갑철관위염독대소서간장초양화물기화매(SOD)활력화병이철(MDA)함량적영향.방법 ICR소서30지,자웅각반,수궤분위3조,매조10지,자웅각반,염독제량위:0、5、20 mg/kg체중,용관위적방법급여갑철,매천1차,련속5d,대조조급여증류수.취간장,용시제합측정각제량조SOD활력화MDA함량.결과 여대조조비교,20 mg/kg염독조소서간장중SOD활력명현강저,MDA적함량명현승고,차이유통계학의의(P<0.05),여대조조비교,20 mg/kg염독조소서간장장기계수명현승고,차이유통계학의의(P<0.05).결론 갑철관위염독대소서간장적지질과양화반응적평형상태구유파배작용,사기항양화능력명현강저.
Objective To study the effects of intragastric administration of formaldehyde on lipid peroxidation in mice.Methods Thirty ICR mice were randomly divided into 3 groups:one control group and two experimental groups.The mice were given formaldehyde (the dose is 0,5 and 20 mg/kg body weight respectively) through intragastric administration once a day for 5 days,and then they were killed.The activities of SOD and the contents of MDA in liver were measured.Results The activities of SOD in the 20 mg/kg body weight group were significantly lower than the control group (P<0.05),and the contents of MDA in the 20 mg/kg body weight group were significantly higher than the control group (P<0.05),and the liver organ coefficient in the 20mg/kg body weight group is higher than the control group (P<0.05).Conclusion A certain dose of formaldehyde can destroy the balance of lipid peroxidation in mice,the ability of antioxidation is reduced obviously,and the liver become compensatory hypertrophy.