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
2010年
5期
345-349
,共5页
潘小海%孙锴%潘家祜%金泰廙
潘小海%孫鍇%潘傢祜%金泰廙
반소해%손개%반가호%금태이
镉%肾%线粒体%膜电位%自由基
鎘%腎%線粒體%膜電位%自由基
력%신%선립체%막전위%자유기
Cadmium%Kidney%Mitochondria%Membrane potentials%Free radicals
目的 研究急性镉染毒对大鼠肾脏线粒体形态和功能的影响.方法 健康成年雄性SD大鼠随机分为4组,每组6只.分别给予大鼠皮下注射染镉0.6、1.2、1.8 mg/kg(CdCl2),对照组注射相应容积生理盐水,每天1次,连续注射5 d.用透射电子显微镜观察肾脏线粒体超微结构变化,差速离心法制备大鼠肾脏线粒体,Clark氧电极法测定线粒体呼吸功能,荧光法测定线粒体膜电位,分光光度法测定线粒体肿胀,四唑盐(NBT)法测定线粒体超氧化物含量.结果 电子显微镜观察显示,镉染毒对大鼠肾脏线粒体的损伤明显,表现为线粒体基质空泡增多、线粒体肿胀色泽加深.随染毒剂量的增加,大鼠肾脏线粒体损伤加重.与对照组相比,高剂量组线粒体Ⅲ态呼吸速率(V3)[(6.25±0.61)nmol/L O2·min-·mg-1]明显低于对照组[(9.66±1.16)nmol/L O2·min-·mg-1],RCR值(2.453±0.23)亦明显降低,差异均有统计学意义(P＜0.01,P＜0.05),提示线粒体呼吸功能受阻;线粒体膜电位水平(85.89%±3.82%)明显低于对照组(100.00%±3.43%),差异有统计学意义(P＜0.05),而氧自由基水平(116.33%±3.06%)则较对照组(100.00%±2.25%)明显上升,差异亦有统计学意义(P＜0.05).结论 急性镉染毒可造成大鼠肾脏线粒体损伤,引起线粒体呼吸功能受阻,膜电位降低,肿胀程度加剧,而这些损伤效应可能与线粒体内氧自由基水平增加有关.
目的 研究急性鎘染毒對大鼠腎髒線粒體形態和功能的影響.方法 健康成年雄性SD大鼠隨機分為4組,每組6隻.分彆給予大鼠皮下註射染鎘0.6、1.2、1.8 mg/kg(CdCl2),對照組註射相應容積生理鹽水,每天1次,連續註射5 d.用透射電子顯微鏡觀察腎髒線粒體超微結構變化,差速離心法製備大鼠腎髒線粒體,Clark氧電極法測定線粒體呼吸功能,熒光法測定線粒體膜電位,分光光度法測定線粒體腫脹,四唑鹽(NBT)法測定線粒體超氧化物含量.結果 電子顯微鏡觀察顯示,鎘染毒對大鼠腎髒線粒體的損傷明顯,錶現為線粒體基質空泡增多、線粒體腫脹色澤加深.隨染毒劑量的增加,大鼠腎髒線粒體損傷加重.與對照組相比,高劑量組線粒體Ⅲ態呼吸速率(V3)[(6.25±0.61)nmol/L O2·min-·mg-1]明顯低于對照組[(9.66±1.16)nmol/L O2·min-·mg-1],RCR值(2.453±0.23)亦明顯降低,差異均有統計學意義(P＜0.01,P＜0.05),提示線粒體呼吸功能受阻;線粒體膜電位水平(85.89%±3.82%)明顯低于對照組(100.00%±3.43%),差異有統計學意義(P＜0.05),而氧自由基水平(116.33%±3.06%)則較對照組(100.00%±2.25%)明顯上升,差異亦有統計學意義(P＜0.05).結論 急性鎘染毒可造成大鼠腎髒線粒體損傷,引起線粒體呼吸功能受阻,膜電位降低,腫脹程度加劇,而這些損傷效應可能與線粒體內氧自由基水平增加有關.
목적 연구급성력염독대대서신장선립체형태화공능적영향.방법 건강성년웅성SD대서수궤분위4조,매조6지.분별급여대서피하주사염력0.6、1.2、1.8 mg/kg(CdCl2),대조조주사상응용적생리염수,매천1차,련속주사5 d.용투사전자현미경관찰신장선립체초미결구변화,차속리심법제비대서신장선립체,Clark양전겁법측정선립체호흡공능,형광법측정선립체막전위,분광광도법측정선립체종창,사서염(NBT)법측정선립체초양화물함량.결과 전자현미경관찰현시,력염독대대서신장선립체적손상명현,표현위선립체기질공포증다、선립체종창색택가심.수염독제량적증가,대서신장선립체손상가중.여대조조상비,고제량조선립체Ⅲ태호흡속솔(V3)[(6.25±0.61)nmol/L O2·min-·mg-1]명현저우대조조[(9.66±1.16)nmol/L O2·min-·mg-1],RCR치(2.453±0.23)역명현강저,차이균유통계학의의(P＜0.01,P＜0.05),제시선립체호흡공능수조;선립체막전위수평(85.89%±3.82%)명현저우대조조(100.00%±3.43%),차이유통계학의의(P＜0.05),이양자유기수평(116.33%±3.06%)칙교대조조(100.00%±2.25%)명현상승,차이역유통계학의의(P＜0.05).결론 급성력염독가조성대서신장선립체손상,인기선립체호흡공능수조,막전위강저,종창정도가극,이저사손상효응가능여선립체내양자유기수평증가유관.
Objective To evaluate effect of acute cadmium administration on mitochondria from rat kidney. Methods 24 male Spragne-Dawley (SD) rats were randomly divided into four groups. Four groups of rats were injected with saline, 0.6, 1.2, and 1.8 mg/kg weight subcutaneously,once daily, for 5 days, respectively. Ultrastructural change of rat kidney mitochondria was observed, and respiration function, membrane potential, mitochondria swelling, and superoxide level were determined. Results Ultrastructural changes included matrix vacuolation, swelling and condensation of mitochondria. In group of 1.8 mg/kg body weight, the oxygen consumption rate during state 3 respiration[(6.25±0.61)nmol/L O2·min-1·mg-1]and RCR value (2.45±0.23)were significantly lower than those of control group[(9.66±1.16)nmol/L O2·min-1·mg-1](P＜0.05).indicating respiration inhibition.The membrane potential and superexide level of the sanle group were 85.89％±3.82％and 116.33％±3.06％ of control values(P＜0.05),respectively.Conclusions Acute cadmium administration can cause rat kidney mitochondrial damage in a dose-effect manner,including inhibition of respiration,dissipation of membrane potential,swelling of mitochondria matrix.Such damage might be related to the increase of mitoehondrial free radical.
