摘要
本实验以游泳训练的大鼠为实验模型 ,观察雄性SD大鼠的肝脏GSH、GSSG的含量以及GSH/GSSG的比值 ,发现一次急性力竭运动后 ,肝脏的GSH含量显著下降 ,P <0 .0 0 1,GSSG的含量显著升高 ,肝脏的GSH/GSSG的比值降低 ,P <0 .0 5 ,GSH/GSSG氧化还原缓冲作用改变的可能性增加影响了细胞信号传递过程。通过对应激激酶富含半胱氨酸结构域的磷酸化作用 ,激活应激激酶 (JNK、p3 8) ,也可激活神经鞘氨醇酶传导途径以及激活转录因子AP -1和NF -κB .最终可能导致某些特定基因转录增加。经十周递增负荷的游泳训练后 ,大鼠肝脏中GSH含量增加 ,P <0 .0 5 ,P <0 .0 0 1。GSSG含量没有变化 ,GSH/GSSG有增加的趋势 ,但无统计学意义。本实验还观察了大鼠肝脏中巯基含量 ,发现巯基与GSH的变化相一致 ,从侧面反映运动导致机体活性氧产生增加 ,细胞氧化还原状态发生改变。
The effects of 10 weeks progressive training and exhaustive exercise on GSH, GSSG content and GSH/GSSG ratio were studied. After one time exhausted exercise glutathione in liver was significant decreased, GSSG content increased and GSH/GSSG ratio in liver significantly decreased. This results suggested that reactive oxygen species be generated during strenuous exercise as a result of the increased oxygen consumption. It influenced the GSH levels by altering the activity of glutathione peroxidase and further generated GSSG and potentially altered the GSH/GSSG equilibrium. The shift in the GSH/GSSG equilibrium influences many cellular signaling processes, such as the activation and phosphorylation of stress kinases (JUK, p38) via sensitive cysteine-rich domains, the activation of sphingomyelinase cerumide pathway, and the activation of the transcription factors AP-1 and NF-κB,eventually leads to an increased gene transcription. GSH content in liver and DVL increased after 10 weeks progressive training while the GSSG content did not significantly changed. GSH/GSSG has a tendency of increase, but no statistics significance was found. Heart GSH content also had a tendency of decrease after 10 weeks progressive training. The change of thiol content in liver, heart and DVL matched the change of GSH. It evidenced the increase reactive oxygen species generation caused by strenuous exercise.
出处
《体育与科学》
CSSCI
北大核心
2004年第1期60-63,34,共5页
Sports & Science
