Department of Zoophysiology, University of Göteborg, Box 25059, S-400 31, Göteborg, Sweden.
Fish Physiol Biochem. 1986 May;1(2):105-11. doi: 10.1007/BF02290210.
The cytochrome P-450 content in liver cells from rainbow trout was not affected by starvation for 12 weeks whereas the rate of cytochrome P-450-dependent deethylation of 7-ethoxycoumarin in liver cells from 6 or 12 weeks starved fish was 60% of the rate in fed fish. Treatment of fish with β-naphthoflavone increased the 7-ethoxycoumarin metabolism several-fold in both starved and fed fish.Optimal cytochrome P-450 monooxygenation in liver cells from fed or starved fish was not affected by addition of glucose or 2-bromooctanoate, an inhibitor of fatty acid β-oxidation which is the main source of metabolic fuel in trout liver. The cellular content of NADPH, an obligatory cofactor for cytochrome P-450 monooxygenation, was not affected by addition of substrate to cytochrome P-450, inhibition of fatty acid β-oxidation or inhibition of the oxidative phosphorylation. This indicates a great capacity of rainbow trout liver cells to retain high NADPH/NADP(+) ratios. These results suggest that the cytochrome P-450 mediated metabolism of xenobiotics in liver cells from fed or starved trout is not limited by the availability of reducing equivalents.
肝组织细胞色素 P-450 含量不受 12 周饥饿影响，然而，饥饿 6 或 12 周鱼的肝组织细胞色素 P-450 依赖性 7-乙氧基香豆素去乙基化速度仅为饱食鱼的 60%。β-萘黄酮处理可使饥饿和饱食鱼的 7-乙氧基香豆素代谢增加几倍。饱食或饥饿鱼肝组织细胞色素 P-450 单加氧酶的最佳活性不受葡萄糖或 2-溴辛酸（脂肪酸β-氧化的抑制剂，也是虹鳟肝脏主要代谢燃料）的影响。细胞色素 P-450 的辅因子 NADPH 的细胞含量不受添加底物、脂肪酸β-氧化抑制或氧化磷酸化抑制的影响。这表明虹鳟鱼肝组织细胞具有保持高 NADPH/NADP(+) 比值的巨大能力。这些结果表明，饱食或饥饿虹鳟鱼肝组织细胞色素 P-450 介导的外源化学物代谢不受还原当量可用性的限制。
