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Effect Of Feeding Acety-l-carnitine And Lipoic Acid On Mitochondrial Permeability Transition Pore In Rats After Endurance Training

Posted on:2009-09-17Degree:MasterType:Thesis
Country:ChinaCandidate:Z G HuFull Text:PDF
GTID:2167360245973975Subject:Human Movement Science
Abstract/Summary:PDF Full Text Request
Mitochondria is the center of the process of cell apoptosis,and this promotion of cell apoptosis is operated by a pore on the mitochondrial membrane-- mitochondrial permeability transition pore(MPTP).MPTP low permeability open is very important on normal physiological function of mitochondria and cell.It regulates cell calcium balance,prevents mitochondrial calcium over loading,transport ATP/ADP.But MPTP high permeability open is a pathological open,it will induce mitochondrial membrane electricity decrease,ATP crock up,oxidative phosphorylation lose coupling, mitochondria dwelling,out membrane broken,release of apoptosis induced factor, and so on,and then cause cell apoptosis or cell death.High intense exercise will induce the production of ROS sharp increase.If this ROS can't be eliminated in time,ROS will accumulate.High concentration ROS is a efficient MPTP revulsant.It will cause MPTP high permeability open.The mechanism of ROS cause MPTP open maybe through exhausting reduced form GSH or NADPH,or maybe through attack -SH on ANT,cause M conformation of ANT transfer to C conformation,then induce MPTP open.ALCAR has the function of stabilizing cell membrane and boosting up cell membrane fastness to ROS;LA is a strong ROS elimination,both ALCAR and LA can increase the content of GSH.Then in front of the attack of ROS,on one hand,feeding ALCAR and LA can eliminate ROS,increase antioxidant capacity,on the other hand,it can repair mitochondrial membrane.So feeding ALCAR and LA can interdict the approach of ROS induced MPTP open.The article through feeding ALCAR and LA to male SD mice for 6 weeks to observe the effect of feeding ALCAR and LA to endurance training mice MPTP. Method:24 SD mice divided into three group in random,contrast group,training group and training & feeding group.All mice engaged in swimming training for 6weeks,6 times per week.UV—Spectrometer detect PTP open,fluorometer detect mitochondrial membrane electricity,double beam Spectrometer detect Ca2+transport. Result:Feeding ALCAR and LA could control the increase of weight obviously; restrain MPTP high permeability open and losing of mitochondrial membrane electricity induced by H2O2;prevent mitochondrial take too much Ca2+. Conclusion:(1)Feeding ALCAR and LA could control the increase of weight obviously by increasing fat energy metabolism and decreasing oxidative stress (2)Endurance training may cause MPTP low permeability open,and this is beneficial to mitochondrial exchange of material.(3)High concentration H2O2 can cause MPTP open,and feeding ALCAR and LA can interdict MPTP open,protect mitochondria structure and function integrality.(4)Feeding ALCAR and LA can interdict mitochondria take too many calcium, maintain the balance of mitochondrial calcium.
Keywords/Search Tags:acetyl-L-catnitine, a-lipoic acid, mitochondrial permeability transition pore, endurance training, membrane potential, calcium transport
PDF Full Text Request
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