INORGANIC PYROPHOSPHATE IS LOCATED PRIMARILY IN THE MITOCHONDRIA OF THE HEPATOCYTE AND INCREASES IN PARALLEL WITH THE DECREASE IN LIGHT-SCATTERING INDUCED BY GLUCONEOGENIC HORMONES, BUTYRATE AND IONOPHORE A23187

INORGANIC PYROPHOSPHATE IS LOCATED PRIMARILY IN THE MITOCHONDRIA OF THE HEPATOCYTE AND INCREASES IN PARALLEL WITH THE DECREASE IN LIGHT-SCATTERING INDUCED BY GLUCONEOGENIC HORMONES, BUTYRATE AND IONOPHORE A23187
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DOI:
10.1042/bj2540379
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发表时间:
1988-09-01
影响因子:
4.1
通讯作者:
HALESTRAP, AP
HALESTRAP, AP
中科院分区:
生物学3区
文献类型:
--
作者:
DAVIDSON, AM;HALESTRAP, AP

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1. The effects of a variety of hormones on the PPi content and light-scattering of isolated rat liver cells was studied. 2. The basal PPi content was about 130 pmol/mg of cell proein, and increased after hormone addition, in parallel with a decrease in light-scattering which we have observed previously [Quinlan, Thomas, Armston and Halestrap (19830 Biochem. J. 214, 295-404]. 3. The mean increases in PPi content with the agonists shown (as pmol/mg of protein) were: 0.1 .mu.M-glucagon, 25; 20 .mu.M-phenylephrine, 30; 25 nM-vasopressin, 127; glucagon + phenylephrine, 115; glucagon + vasopressin, 382; 100 .mu.M-ADP, 50; 15 .mu.M-A23187, 72; 1 mM-butyrate, 80.4. In the absence of extracellular Ca2+, vasopressin had little effect on either the PPi content or the light-scattering of hepatocytes. 5. The magnitude of the increase in PPi content correlated with that of the decrease in light-scattering irrespective of the stimulating agent, provided that the PPi did not exceed 300 pmol/mg of protein. Above this value little additional change in light-scattering was observed. 6. Subcellular fractionation showed that over 90% of the cellular PPi was intramitochondrial in both control and stimulated cells. 7. The data support the conclusions of previous experiments using isolated liver mitochondria [Davidson and Halestrap (1987) Biochem. J. 246, 715-723] that hormones increase the mitochondrial matrix volume through a Ca2+-induced rise in matrix [PPi]. 8. It is further proposed that this increase in mitochondrial [PPi] allows entry of ADP into the mitochondria in exchange for PPi and is therefore responsible for the increase in total mitochondrial adenine nucleotides observed after hormone treatment.