pThe turnover of the adenine nucleotide pool, the pathway of the degradation of AMP and the occurrence of recycling of adenosine were investigated in isolated chicken hepatocytes, in which the adenylates had been labelled by prior incubation with [14C]adenine. Under physiological conditions, 85% of the IMP synthesized by the ‘de novo’ pathway (approx. 37 nmol/min per g of cells) was catabolized directly via inosine into uric acid, and 14% was converted into adenine nucleotides. The latter were found to turn over at the rate of approx. 5 nmol/min per g of tissue. Inhibition of adenosine deaminase by 1 microM-coformycin had no effect on the formation of labelled uric acid, indicating that the initial degradation of AMP proceeds by way of deamination rather than dephosphorylation. Inhibition of adenosine kinase by 100 microM-5-iodotubercidin resulted in a loss of labelled ATP, demonstrating that adenosine is normally formed from AMP but is recycled. Unexpectedly, 5-iodotubercidin did not decrease the total concentration of ATP, indicating that the loss of adenylates caused by inhibition of adenosine kinase was nearly completely compensated by formation of AMP de novo. Anoxia induced a greatly increased catabolism of the adenine nucleotide pool, which proceeded in part by dephosphorylation of AMP. On reoxygenation, the formation of AMP de novo was increased 8-fold as compared with normoxic conditions. The latter results indicate the existence of adaptive mechanisms in chick liver allowing, when required, channelling of the metabolic flux through the ‘de novo’ pathway, away from the uricotelic catabolic route, into the synthesis of adenine nucleotides./p
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机译：>在分离的鸡肝细胞中研究了腺嘌呤核苷酸库的周转率，AMP降解的途径和腺苷循环的发生，其中通过与[14C]腺嘌呤预先孵育来标记腺苷酸。在生理条件下，通过“从头”途径合成的IMP的85％（每克细胞约37 nmol / min）直接通过肌苷分解为尿酸，而14％转化为腺嘌呤核苷酸。后者被发现以大约1/3的速率翻转。每克组织5 nmol / min。 1 microM-coformycin对腺苷脱氨酶的抑制作用对标记尿酸的形成没有影响，表明AMP的初始降解是通过脱氨而不是去磷酸化进行的。 100 microM-5-iodotubercidin对腺苷激酶的抑制作用会导致标记的ATP丢失，这表明腺苷通常由AMP形成，但可以回收利用。出乎意料的是，5-碘代小球蛋白并没有降低ATP的总浓度，表明由腺苷激酶抑制引起的腺苷酸损失几乎完全由AMP de novo形成所补偿。缺氧诱导腺嘌呤核苷酸库的分解代谢大大增加，其部分通过AMP的去磷酸化进行。与正常氧条件相比，复氧后AMP de novo的形成增加了8倍。后一项结果表明，鸡肝中存在适应性机制，从而可以在需要时通过“从头”途径将代谢通量从尿酸分解代谢途径引导到腺嘌呤核苷酸的合成中。
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