Functional replacement of oxygen by other oxidants in articular cartilage
Functional replacement of oxygen by other oxidants in articular cartilage
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DOI：
10.1002/art.10686
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发表时间：
2002-12-01
影响因子：
--
通讯作者：
Urban, JPG
中科院分区：
文献类型：
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作者：
Lee, RB;Urban, JPG
目标。与大多数其他动物细胞相比，关节软骨软骨细胞消耗的O-2非常少；糖酵解形成了软骨中ATP的主要来源。尽管在许多天内不会致死，但施加缺氧会立即降低细胞内ATP，抑制糖酵解速率，并阻止关节软骨细胞产生细胞外基质大分子。本研究旨在探讨O-2在关节软骨细胞代谢中的作用。我们检查了氧和其他几种外源性氧化剂的影响，即1)染料亚甲基蓝和2,6-二氯苯酚-吲哚酚，2)铁（III）络合物铁氰化物，以及3)酮酸草酰乙酸和丙酮酸（以及磷酸烯醇丙酮酸，丙酮酸的代谢前体），对体外牛关节软骨糖酵解速率和硫酸盐结合的影响。乳酸产量在缺氧条件下最低，并通过添加O-2（空气饱和介质）刺激数倍。在严格缺氧条件下，其他氧化剂将乳酸生成恢复到至少与有氧对照相当的速率；在有氧条件下，它们几乎没有效果。氧和其他氧化剂对硫酸盐掺入的刺激比乳酸的产生更强烈。在缺氧条件下，促进糖酵解和硫酸盐在软骨中掺入的化合物本身也减少了；也就是说，它们是代替o -2的氧化剂。为了正常功能，关节软骨似乎需要外源性氧化剂来刺激糖酵解并产生ATP和细胞外基质。在生理条件下，氧充当这种氧化剂，但它的作用可以由其他试剂充分承担。
Objective. Articular cartilage chondrocytes consume remarkably little O-2 in comparison with most other animal cells; glycolysis forms the principal source of ATP in this cartilage. Although not lethal for many days, imposition of anoxia immediately lowers intracellular ATP, inhibits rates of glycolysis, and prevents articular chondrocytes from producing extracellular matrix macromolecules. This study was undertaken to investigate the role of O-2 in articular chondrocyte metabolism.Methods. We examined the effects of oxygen and of several other classes of exogenous oxidants, i.e., 1) the dyes methylene blue and 2,6-dichlorophenol-indophenol, 2) the iron (III) complex ferricyanide, and 3) the keto-acids oxaloacetate and pyruvate (and phosphoenolpyruvate, a metabolic precursor of pyruvate), on rates of glycolysis and of sulfate incorporation by bovine articular cartilage in vitro.Results. Lactate production was lowest under conditions of anoxia and was stimulated severalfold by addition of O-2 (air-saturated medium). Under strict anoxia, other oxidants restored lactate production to rates at least comparable with those seen in aerobic controls; under aerobic conditions, they had little effect. Oxygen and all of the other oxidants examined stimulated sulfate incorporation more strongly than lactate production. The compounds that promoted glycolysis and hence sulfate incorporation in cartilage under anoxia were themselves reduced; that is, they functioned as oxidants in lieu of O-2.Conclusion. For normal function, articular cartilage appears to require exogenous oxidants to stimulate glycolysis and produce ATP and extracellular matrix. Under physiologic conditions, oxygen acts as this oxidant, but its role can be adequately assumed by other agents.