天津医药
天津醫藥
천진의약
Tianjin Medical Journal
2015年
10期
1119-1121
,共3页
肖元梅%徐群英%张中伟%李伟%冯建高%任清风%任晓慧%李炜娟
肖元梅%徐群英%張中偉%李偉%馮建高%任清風%任曉慧%李煒娟
초원매%서군영%장중위%리위%풍건고%임청풍%임효혜%리위연
铅%过氧化氢%丙二醛%羟自由基%脂质过氧化作用%脑组织%大鼠, Sprague-Dawley
鉛%過氧化氫%丙二醛%羥自由基%脂質過氧化作用%腦組織%大鼠, Sprague-Dawley
연%과양화경%병이철%간자유기%지질과양화작용%뇌조직%대서, Sprague-Dawley
lead%hydrogen peroxide%malondialdehyde%hydroxyl radical%lipid peroxidation%brain tissue%rats,Sprague-Dawley
目的:探讨乙酸铅对大鼠大脑皮质、小脑、海马组织自由基和脂质过氧化的影响。方法48只刚断乳雄性SD大鼠,按体质量采用随机区组法分为4组(对照组和低、中、高剂量组),对照组大鼠饮用去离子水,低、中、高剂量组分别饮用200、400、800 mg/L的乙酸铅溶液。连续染毒60 d后,取血进行血铅测定,取各组脑组织(大脑皮质、小脑和海马)进行羟自由基抑制活力、过氧化氢(H2O2)水平及丙二醛(MDA)含量的测定。结果与对照组相比,各染铅组大鼠血铅含量显著升高,大脑皮质、小脑和海马组织羟自由基抑制活力明显下降,且随染铅剂量的升高呈逐渐下降趋势(P<0.05);大脑皮质、小脑和海马组织H2O2水平及MDA含量高于对照组,并随着染铅剂量的升高呈逐渐升高趋势(P<0.05);大脑皮质、小脑和海马组织的羟自由基抑制活力与血铅含量呈负相关(r分别为-0.505、-0.414、-0.448,P<0.05),H2O2和MDA含量均与血铅含量呈正相关(r分别为0.301、0.411、0.378和0.404、0.324、0.510,P<0.05)。结论铅可通过诱发自由基产生,导致大鼠脑组织发生脂质过氧化反应。
目的:探討乙痠鉛對大鼠大腦皮質、小腦、海馬組織自由基和脂質過氧化的影響。方法48隻剛斷乳雄性SD大鼠,按體質量採用隨機區組法分為4組(對照組和低、中、高劑量組),對照組大鼠飲用去離子水,低、中、高劑量組分彆飲用200、400、800 mg/L的乙痠鉛溶液。連續染毒60 d後,取血進行血鉛測定,取各組腦組織(大腦皮質、小腦和海馬)進行羥自由基抑製活力、過氧化氫(H2O2)水平及丙二醛(MDA)含量的測定。結果與對照組相比,各染鉛組大鼠血鉛含量顯著升高,大腦皮質、小腦和海馬組織羥自由基抑製活力明顯下降,且隨染鉛劑量的升高呈逐漸下降趨勢(P<0.05);大腦皮質、小腦和海馬組織H2O2水平及MDA含量高于對照組,併隨著染鉛劑量的升高呈逐漸升高趨勢(P<0.05);大腦皮質、小腦和海馬組織的羥自由基抑製活力與血鉛含量呈負相關(r分彆為-0.505、-0.414、-0.448,P<0.05),H2O2和MDA含量均與血鉛含量呈正相關(r分彆為0.301、0.411、0.378和0.404、0.324、0.510,P<0.05)。結論鉛可通過誘髮自由基產生,導緻大鼠腦組織髮生脂質過氧化反應。
목적:탐토을산연대대서대뇌피질、소뇌、해마조직자유기화지질과양화적영향。방법48지강단유웅성SD대서,안체질량채용수궤구조법분위4조(대조조화저、중、고제량조),대조조대서음용거리자수,저、중、고제량조분별음용200、400、800 mg/L적을산연용액。련속염독60 d후,취혈진행혈연측정,취각조뇌조직(대뇌피질、소뇌화해마)진행간자유기억제활력、과양화경(H2O2)수평급병이철(MDA)함량적측정。결과여대조조상비,각염연조대서혈연함량현저승고,대뇌피질、소뇌화해마조직간자유기억제활력명현하강,차수염연제량적승고정축점하강추세(P<0.05);대뇌피질、소뇌화해마조직H2O2수평급MDA함량고우대조조,병수착염연제량적승고정축점승고추세(P<0.05);대뇌피질、소뇌화해마조직적간자유기억제활력여혈연함량정부상관(r분별위-0.505、-0.414、-0.448,P<0.05),H2O2화MDA함량균여혈연함량정정상관(r분별위0.301、0.411、0.378화0.404、0.324、0.510,P<0.05)。결론연가통과유발자유기산생,도치대서뇌조직발생지질과양화반응。
Objective To explore the effects of lead acetate on free radicals and lipid peroxidation in the cerebral cor?tex, cerebellum, and hippocampus in rat brains. Methods SD rats (n=48), who were just weaned, were randomly divided in?to 4 groups base on their weight. Then the rats were fed with lead acetate in drinking water at the final concentrations of 0 mg/L (deionized water), 200 mg/L, 400 mg/L, 800 mg/L respectively. Blood lead level as well as the hydroxyl free radical inhibiting activity, the levels of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in cerebral cortex, cerebellum, and hippocam?pus were measured 60 days after lead contamination in water. Results Upon lead exposure, blood lead levels increased sig?nificantly as compared with the control. The hydroxyl free radical inhibiting activity in cerebral cortex, cerebellum, and hip?pocampus decreased significantly in a dose dependent manner of lead(P < 0.05). And they all correlated negatively with blood lead level (r=-0.505,-0.414,-0.448, P<0.05). By contrast, blood lead level was positively correlated with H2O2 and MDA in these brain tissues (r=0.301, 0.411, 0.378, and 0.404, 0.324, 0.510,P < 0.05). Conclusion Lead exposure can lead to lipid peroxidation of rat brain tissues through inducing free radicals.