摘要
目的探讨铝中毒对神经细胞线粒体氧化磷酸化功能的影响。方法Wistar大鼠37只,分对照组、氯化铝低剂量组、氯化铝高剂量组,饲养3个月,建立铝中毒模型。氧电极法及华氏(Warburg)检压法测定线粒体的耗氧量、呼吸控制率(RCR)和二磷酸腺苷/氧(ADP/O)比值。以RCR评价线粒体的完整性及程度,用ADP/O评价线粒体氧化磷酸化的效率。结果低剂量组、高剂量组与对照组比较,ADP/O、RCR显著降低(P<0.01),高剂量组与低剂量组比较,ADP/O显著降低(P<0.01)。氧电极法呼吸Ⅲ态(R3)耗氧量低剂量组与对照组比较显著升高(P<0.01),高剂量组与低剂量组比较显著降低(P<0.01);呼吸Ⅳ态(R4)耗氧量低剂量组、高剂量组与对照组比较显著升高(P<0.01)。华氏检压法耗氧量低剂量组、高剂量组与对照组比较显著升高(P<0.01),高剂量组与低剂量组比较显著降低(P<0.05)。结论低剂量铝染毒时线粒体氧化磷酸化部分解偶联,脑细胞轻度损伤,为可逆性变化。而高剂量铝染毒时线粒体氧化磷酸化效率很低,脑细胞损伤严重,线粒体损伤十分明显,可能是不可逆性变化。
Objective To study the effect of aluminum poisoning on mitochondrial oxidation phosphorylation of nerve cells. Methods 37 Wistar rats were divided into three groups: low dose aluminum chloride group, high dose aluminum chloride group and control group. All of them were fed for three months to establish aluminum poisoning models. The oxygen consumption capacity, respiratory control rate(RCR) and ADP/O ratio in mitochondria were determined with oxygen electrode and Warburg pressure detector. The mitochondrial integrity and coupling degree were appraised by RCR. The mitochondrial oxidation phosphorylation efficiency was evaluated with ADP/O. Results ADP/O and RCR of low dose aluminum chloride group and high dose aluminum chloride group decreased significantly in contrast to that of the control group (P〈0.01). ADP/O of the high dose aluminum chloride group reduced evidently comparing with that of the low dose aluminum chloride group (P〈0.01). R3 (respiratory stateⅢ ) oxygen consumption capacity by oxygen electrode of the low close aluminum chloride group increased significantly in contrast with that of the control group (P〈0.01), and the low dose and the high dose aluminum chloride groups decreased significantly (P〈0.01). R4(Ⅳ respiratory state) oxygen consumption capacity of the low dose and the high dose aluminum chloride groups increased significantly in contrast to that of the control group (P〈0.01). Oxygen consumption capacity by Warburg pressure detector of the low dose and the high dose aluminum chloride groups increased significantly in contrast to that of the control group (P〈0.01) ; and that of the high dose aluminum chloride group decreased significantly comparing with that of the low dose aluminum chloride group (P〈0.05). Conclusions When the mitochondria are poisoned by low dose aluminum, the oxidation phosphorylation was partially uncoupled. The nerve cells were slightly injured and the changes were reversible. When poisoned by high dose aluminum, the oxidation phosphorylation efficiency was very low. The nerve cells were severely injured; and the mitochondria were very obviously injured and the changes might be irreversible.
出处
《工业卫生与职业病》
CAS
CSCD
北大核心
2009年第2期74-76,共3页
Industrial Health and Occupational Diseases
关键词
铝中毒
线粒体
氧化磷酸化
Aluminum poisoning
Mitochondrion
Oxidative phosphorylation