Mildaziene V, Baniene R, Nauciene Z, Bakker B M, Brown G C, Westerhoff H V, Kholodenko B N
Institute for Biomedical Research, Kaunas Medical Academy, Lithuania.
Arch Biochem Biophys. 1995 Dec 1;324(1):130-4. doi: 10.1006/abbi.1995.9918.
The effect of calcium on the control exerted by the adenine nucleotide translocator over respiration in isolated heart mitochondria was investigated in order to determine whether calcium directly stimulates the translocator. At respiration rates intermediate between states 3 and 4, Ca2+ is shown to increase the control over 2-oxoglutarate oxidation exerted by the adenine nucleotide translocator in rat heart mitochondria. This did not occur when succinate was the respiratory substrate, even though the control exerted by the translocator was substantial, indicating that Ca2+ does not have a direct effect on the adenine nucleotide translocator. Ca2+ increased the uncoupled oxidation rate of 2-oxoglutarate, but not succinate. Using the summation theorem for flux control, the effect of Ca2+ is explained by a shift of the control over respiration rate toward the adenine nucleotide translocator, from the respiratory chain, presumably as the result of the activation of the 2-oxoglutarate dehydrogenase complex.
为了确定钙是否直接刺激腺嘌呤核苷酸转位酶,研究了钙对离体心脏线粒体中腺嘌呤核苷酸转位酶对呼吸作用的控制效果。在状态3和状态4之间的中间呼吸速率下,Ca2+可增强大鼠心脏线粒体中腺嘌呤核苷酸转位酶对2-氧代戊二酸氧化的控制。当琥珀酸作为呼吸底物时,这种情况并未发生,尽管转位酶施加的控制作用很大,这表明Ca2+对腺嘌呤核苷酸转位酶没有直接影响。Ca2+增加了2-氧代戊二酸的解偶联氧化速率,但没有增加琥珀酸的解偶联氧化速率。利用通量控制的叠加定理,Ca2+的作用可以解释为呼吸速率的控制从呼吸链向腺嘌呤核苷酸转位酶转移,这可能是由于2-氧代戊二酸脱氢酶复合体的激活所致。