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The Damage of Mitochondra in the Chronic Alcoholic Myopathy

Author: QiShanShan
Tutor: WangJianFeng
School: Dalian Medical University
Course: Neurology
Keywords: Chronic alcoholic myopathy Mitochondria Mitochondrial membrane fluidity Mitochondrial membrane potential Cytochrome C
CLC: R595.6
Type: Master's thesis
Year: 2009
Downloads: 60
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Abstract


Chronic alcoholic myopathy (Chronic alcoholic myopathy, CAM) is caused by a muscle disease due to chronic alcoholism, the main clinical manifestations of muscle weakness, muscle pain and muscle atrophy, seriously affect the quality of life of the patients. Studies have shown that oxidation - antioxidative status imbalances affect the occurrence and development of CAM, reactive oxygen species (ROS) plays a vital role in the oxidation - antioxidant status imbalances. Mitochondria are important organelles in the cell, it functions in addition to ATP production in recent years also found that reactive oxygen species (ROS) generated within the mitochondria and the cell-related. Mitochondria is both the site of ROS production and ROS damage cells. Studies at home and abroad on the chronic alcoholic myopathy mitochondria for ATP synthesis, mitochondrial damage has not been found reported. This paper analyzes the chronic alcoholic myopathy in mitochondrial damage and oxidative imbalance in the relationship - antioxidant status, to further investigate the pathogenesis of the disease. Objective: To establish a rat chronic alcoholic myopathy model measured antioxidant indicators of chronic alcoholic myopathy pathogenesis of skeletal muscle tissue oxidation, mitochondrial membrane fluidity, mitochondrial cytochrome c levels and mitochondrial transmembrane potential changes to study mitochondrial damage in chronic alcoholic myopathy and investigate the cause of the damage, to study the pathogenesis of chronic alcoholic myopathy, which provide reliable experimental basis for clinical treatment of the disease. Methods: Health SPF level female and male SD rats were 60, were randomly divided into two groups (control group, the experimental group), each group were fed with improved nutrition high fat diet, observed before and after the experiment rats weight, behavior Histological changes. After 12 weeks, take the hind legs plantaris muscle, confirmed by staining method mode. Application spectrophotometer detection muscle tissue antioxidant indicators (SOD, GSH-Px, MDA) content analysis of skeletal muscle oxidation - antioxidative status. Through the the fluorescence spectrophotometer mitochondrial membrane fluidity changes as well as Western Blot mitochondrial membrane protein cytochrome c. Application of flow cytometry mitochondrial membrane potential. Results: 1. Beginning of the experiment was no significant difference in body weight of rats; significant difference experiment the late experimental group body weight of rats with the control group; biochemical detection results: MDA content in rat skeletal muscle (plantar) of the experimental group was significantly high in the control group; SOD, GSH-Px activity was measured experimental group than the control group; mitochondrial membrane fluidity change: the experimental group rat skeletal muscle (plantaris) microviscosity was significantly higher than the control group; 4. cytochrome c change of expression: the experimental group rat skeletal muscle (plantaris) decrease in protein content; 5. changes in mitochondrial membrane potential: rat skeletal muscle (plantar) of the experimental group compared with the control group significantly reduced. Conclusions: 1. Chronic alcoholic myopathy mitochondrial injury, tips and ROS-related increase. ROS increased the mitochondrial membrane fluidity decreased mitochondrial membrane cytochrome c content decreased mitochondrial membrane potential. Chronic alcoholic myopathy of skeletal muscle mitochondrial membrane fluidity decreased, reflecting the impairment of membrane proteins. 3. Decrease in mitochondrial membrane cytochrome c content, mitochondrial membrane potential prompts mitochondrial damage, 02 - and increased production.

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CLC: > Medicine, health > Internal Medicine > Systemic disease > Poisoning and chemical damage > Alcohol poisoning
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