Terada L S, Beehler C J, Banerjee A, Brown J M, Grosso M A, Harken A H, McCord J M, Repine J E
Department of Medicine, University of Colorado, Denver 80262.
J Appl Physiol (1985). 1988 Nov;65(5):2349-53. doi: 10.1152/jappl.1988.65.5.2349.
Xanthine oxidase (XO) and xanthine dehydrogenase (XD) activities decreased in lungs isolated from rats and cultured lung endothelial cells that had been exposed to hyperoxia. Purified XO activity also decreased after addition of a variety of chemically generated O2 metabolite species (superoxide anion, hydrogen peroxide, hydroxyl radical, or hypochlorous acid), hypoxanthine, or stimulated neutrophils in vitro. XO inactivation by chemically, self-, or neutrophil-generated O2 metabolites was decreased by simultaneous addition of various O2 metabolite scavengers but not their inactive analogues. Since XO appears to contribute to a variety of biological processes and diseases, hyperoxia- or O2 metabolite-mediated decreases in XO activity may be an important cellular control mechanism.
在暴露于高氧环境的大鼠分离肺组织和培养的肺内皮细胞中，黄嘌呤氧化酶（XO）和黄嘌呤脱氢酶（XD）的活性降低。在体外添加多种化学产生的氧代谢产物（超氧阴离子、过氧化氢、羟基自由基或次氯酸）、次黄嘌呤或刺激的中性粒细胞后，纯化的XO活性也降低。通过同时添加各种氧代谢产物清除剂而非其无活性类似物，可减少化学、自身或中性粒细胞产生的氧代谢产物对XO的失活作用。由于XO似乎参与多种生物学过程和疾病，高氧或氧代谢产物介导的XO活性降低可能是一种重要的细胞控制机制。
