POSTNATAL-DEVELOPMENT OF RAT-LIVER MITOCHONDRIA - STATE-3 RESPIRATION, ADENINE-NUCLEOTIDE TRANSLOCASE ACTIVITY, AND THE NET ACCUMULATION OF ADENINE-NUCLEOTIDES
POSTNATAL-DEVELOPMENT OF RAT-LIVER MITOCHONDRIA - STATE-3 RESPIRATION, ADENINE-NUCLEOTIDE TRANSLOCASE ACTIVITY, AND THE NET ACCUMULATION OF ADENINE-NUCLEOTIDES
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DOI：
10.1016/0003-9861(80)90546-9
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发表时间：
1980-01-01
影响因子：
3.9
通讯作者：
ASIMAKIS, GK
中科院分区：
文献类型：
--
作者：
APRILLE, JR;ASIMAKIS, GK
研究了从妊娠第22天剖腹产的新生大鼠肝脏中分离的线粒体的呼吸活性的出生后成熟。出生时，状态3呼吸频率与谷氨酸+苹果酸（68.1 .+-. 8.4 ng原子O/min/mg蛋白质）远低于2，4-二硝基苯酚-解偶联速率（112.7 ± 0.001）。13.3 ng原子0/min/mg蛋白质）。在出生后的第一个小时，状态3率增加到几乎等于未偶联率，这并没有显着变化。状态4速率和ADP/O比率没有变化。出生后1小时，当状态3呼吸增加了1.6倍，总腺嘌呤核苷酸含量（ATP + ADP + AMP）增加了1.8倍，腺嘌呤核苷酸转位酶活性增加了1.5倍。总腺嘌呤核苷酸含量和易位酶活性继续增加1和4.5小时出生后彼此平行，但长后状态3呼吸已发展到最大。在体外研究了新生肝线粒体积累腺嘌呤核苷酸的能力与状态3呼吸成熟的关系。线粒体与1 mM ATP在30 ℃温育。C 10分钟增加了一倍，其总腺嘌呤核苷酸含量，这是与状态3呼吸速率的两倍。腺嘌呤核苷酸的净积累被抑制76 . 100 μ M N-乙基马来酰亚胺为1.8%，而在较小程度上为（57 ± 0.01）%。0.5%）。线粒体内腺嘌呤核苷酸的积累，通过ATP或ADP的净摄取，可能占出生后成熟的腺嘌呤核苷酸转位酶活性和状态3呼吸。易位率变化作为一个功能的一个更大范围的线粒体内腺嘌呤核苷酸含量比整体状态3率。出生时ADP刺激呼吸的低速率可能受到易位酶介导的新合成ATP与外部ADP的交换速率和/或可交换的内部腺嘌呤核苷酸池的绝对大小的限制，这可能是F1-ATP酶的次最大值。
The postnatal maturation of respiratory activity was studied in mitochondria isolated from livers of newborn rats that had been Caeserean delivered on the 22nd day of gestation. At birth, the State 3 respiratory rate with glutamate + malate (68.1 .+-. 8.4 ng atoms O/min per mg protein) was much lower than the 2,4-dinitrophenol-uncoupled rate (112.7 .+-. 13.3 ng atoms O/min per mg protein). During the 1st h of postnatal life, the State 3 rate increased to nearly equal the uncoupled rate, which did not change significantly. The State 4 rate and ADP/O ratio did not change. After 1 h postnatal, when State 3 respiration had increased 1.6-fold, the total adenine nucleotide content (ATP + ADP + AMP) had increased 1.8-fold, and adenine nucleotide translocase activity had increased 1.5-fold. The total adenine nucleotide content and translocase activity continued to increase between 1 and 4.5 h postnatal in parallel with each other, but long after State 3 respiration had developed maximally. The ability of newborn liver mitochondria to accumulate adenine nucleotides in relation to the maturation of State 3 respiration was studied in vitro. Mitochondria incubated with 1 mM ATP at 30.degree. C for 10 min doubled their total adenine nucleotide content, and this was correlated with a doubling of the State 3 respiratory rate. The net accumulation of adenine nucleotides was inhibited 76 .+-. 1.8% by 100 .mu.M N-ethylmaleimide and to a lesser extent (57 .+-. 0.5%) by 50 .mu.M atractyloside. The accumulation of intramitochondrial adenine nucleotides, via the net uptake of ATP or ADP, probably accounted for the postnatal maturation of adenine nucleotide translocase activity and State 3 respiration. The translocase rate varied as a function of a much greater range of intramitochondrial adenine nucleotide contents than did the overall State 3 rate. The low rate of ADP-stimulated respiration at birth may have been limited by the rate of translocase-mediated exchange of newly synthesized ATP for external ADP, and/or by the absolute size of the exchangeable internal adenine nucleotide pool, which may have been submaximal for the F1-ATPase.