Krumschnabel G, Biasi C, Wieser W
Institut für Zoologie, Abteilung für Okophysiologie, Universität Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
J Exp Biol. 2000 Sep;203(Pt 17):2657-65. doi: 10.1242/jeb.203.17.2657.
In a comparative study, we analysed the effects of adenosine on the energetics, protein synthesis and K(+ )homeostasis of hepatocytes from the anoxia-tolerant goldfish Carassius auratus and the anoxia-intolerant trout Oncorhynchus mykiss. The rate of oxygen consumption did not respond immediately to the addition of adenosine to the cells from either species, but showed a significant decrease in trout hepatocytes after 30 min. The anaerobic rate of lactate formation was not significantly affected by adenosine in goldfish hepatocytes, but was increased in trout cells. We also studied the effects of adenosine on the two most prominent ATP consumers in these cells, protein synthesis and Na(+)/K(+)-ATPase activity. Under aerobic conditions, adenosine inhibited protein synthesis of hepatocytes from goldfish by 51% and of hepatocytes from trout by 32%. During anoxia, the rate of protein synthesis decreased by approximately 50% in goldfish hepatocytes and by 90% in trout hepatocytes, and this decrease was not altered by the presence of adenosine. Adenosine inhibited normoxic Na(+)/K(+)-ATPase activity and K(+ )efflux by 20-35% in the cells of both species. An investigation into the mechanism underlying the inhibition of protein synthesis by adenosine indicated that, in the goldfish cells, adenosine acts via a membrane receptor-mediated pathway, i.e. the effect of adenosine was abolished by applying the A1 receptor antagonist 8-phenyltheophylline. In the trout, however, the uptake of adenosine into hepatocytes seems to be required for an effect on protein synthesis. Ca(2+) does not seem to be involved in the inhibition of protein synthesis by adenosine.
在一项比较研究中，我们分析了腺苷对耐缺氧金鱼（Carassius auratus）和不耐缺氧虹鳟（Oncorhynchus mykiss）肝细胞的能量代谢、蛋白质合成及钾离子稳态的影响。向来自这两个物种的细胞中添加腺苷后，氧气消耗速率并未立即出现变化，但30分钟后虹鳟肝细胞中的氧气消耗速率显著下降。腺苷对金鱼肝细胞中乳酸形成的无氧速率没有显著影响，但会使虹鳟细胞中的该速率增加。我们还研究了腺苷对这些细胞中两个最主要的ATP消耗过程，即蛋白质合成和钠钾ATP酶活性的影响。在有氧条件下，腺苷使金鱼肝细胞的蛋白质合成抑制了51%，使虹鳟肝细胞的蛋白质合成抑制了32%。在缺氧期间，金鱼肝细胞中的蛋白质合成速率下降了约50%，虹鳟肝细胞中的下降了90%，且腺苷的存在并未改变这种下降趋势。腺苷使两个物种细胞中的常氧钠钾ATP酶活性和钾离子外流抑制了20 - 35%。对腺苷抑制蛋白质合成的潜在机制进行的研究表明，在金鱼细胞中，腺苷通过膜受体介导的途径发挥作用，即应用A1受体拮抗剂8 - 苯基茶碱可消除腺苷的作用。然而，在虹鳟中，腺苷似乎需要被肝细胞摄取才能对蛋白质合成产生影响。细胞内钙离子浓度似乎不参与腺苷对蛋白质合成的抑制作用。
