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高氧压对钾诱导的大鼠脑片丙酮酸脱氢酶激活及葡萄糖代谢的抑制作用。

Inhibitory effect of high oxygen pressure on potassium- induced activation of pyruvate dehydrogenase and glucose metabolism in rat brain slices.

作者信息

Kovachich G B, Schina M J, Haugaard N

出版信息

Biochim Biophys Acta. 1977 Dec 23;462(3):493-500. doi: 10.1016/0005-2728(77)90096-2.

DOI:10.1016/0005-2728(77)90096-2
PMID:597491
Abstract

The effects of high oxygen pressure on pyruvate dehydrogenase (pyruvate: lipoate oxidoreductase (decarboxylating and acceptor-acylating), EC 1.2.4.1) activity, tissue concentration of ATP, and CO2 production from glucose were studied in rat brain cortical slices. The increase in pyruvate dehydrogenase activity and the lowering of cellular ATP, occurring during potassium-induced depolarization at 1 atm of oxygen, were reversed by increasing the oxygen pressure to 5 atm. When brain slices were incubated at 1 atm oxygen with [U-14C]glucose, a high potassium medium approximately doubled the production of 14CO2. Oxygen at 5 atm abolished this potassium-dependent increase in 14CO2 production with no significant effect on glucose oxidation in normal Krebs-Ringer phosphate medium. Adding 4 atm helium to 1 atm oxygen did not interfere with the ability of potassium ions to activate pyruvate dehydrogenase, lower ATP, or increase glucose oxidation. The results show that toxic effects of hyperbaric oxygen, not manifest in "resting" tissue, may be revealed during stress such as potassium depolarization. The site of the toxic effects of oxygen is probably the cell membrane where excess oxygen appears to interfere with the action of the sodium pump, calcium transport or other processes stimulated by increased concentrations of extracellular potassium.

摘要

在大鼠脑皮质切片中研究了高氧压对丙酮酸脱氢酶(丙酮酸:硫辛酰胺氧化还原酶(脱羧和酰基受体酰化),EC 1.2.4.1)活性、组织ATP浓度以及葡萄糖产生CO2的影响。在1个大气压氧气条件下,钾诱导去极化过程中发生的丙酮酸脱氢酶活性增加和细胞ATP降低,通过将氧压提高到5个大气压而逆转。当脑切片在1个大气压氧气下与[U-14C]葡萄糖一起孵育时,高钾培养基使14CO2的产生量增加了约一倍。5个大气压的氧气消除了这种钾依赖性的14CO2产生增加,而对正常的磷酸 Krebs-Ringer 培养基中的葡萄糖氧化没有显著影响。向1个大气压氧气中添加4个大气压氦气并不干扰钾离子激活丙酮酸脱氢酶、降低ATP或增加葡萄糖氧化的能力。结果表明,高压氧的毒性作用在“静息”组织中不明显,但在钾去极化等应激过程中可能会显现出来。氧的毒性作用部位可能是细胞膜,过量的氧似乎在细胞膜处干扰钠泵的作用、钙转运或其他由细胞外钾浓度增加所刺激的过程。

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Inhibitory effect of high oxygen pressure on potassium- induced activation of pyruvate dehydrogenase and glucose metabolism in rat brain slices.高氧压对钾诱导的大鼠脑片丙酮酸脱氢酶激活及葡萄糖代谢的抑制作用。
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