Ventura C, Guarnieri C, Caldarera C M
Ital J Biochem. 1985 Jul-Aug;34(4):267-74.
The superoxide radicals generated by the xanthine oxidase reaction reduced the myofibrillar Ca2+-ATPase activity. This negative effect was prevented by superoxide dismutase or by dithiothreitol, a protective thiol compound. Partial protection was achieved by catalase, while mannitol was ineffective. The myofibrillar Ca2+-ATPase exposed to O2-. radicals did not modify the affinity for Ca2+ while it showed a remarkable reduction of Vmax measured at the saturating level of Ca2+. The O2-. inhibited myofibrillar ATPase showed a higher value of Km for the cofactor associated to a reduced value of Vmax when studied in the presence of increasing concentration of ATP. Thus, circumstances that enhance the production of cardiac O2- radicals can be considered a negative metabolic event capable of depressing the myofibrillar Ca2+-ATPase activity.
黄嘌呤氧化酶反应产生的超氧阴离子自由基降低了肌原纤维Ca2+-ATP酶活性。超氧化物歧化酶或二硫苏糖醇(一种具有保护作用的硫醇化合物)可防止这种负面影响。过氧化氢酶可实现部分保护,而甘露醇则无效。暴露于O2-自由基的肌原纤维Ca2+-ATP酶对Ca2+的亲和力未发生改变,但其在Ca2+饱和水平下测得的Vmax显著降低。当在ATP浓度不断增加的情况下进行研究时,受O2-抑制的肌原纤维ATP酶对辅助因子的Km值较高,而Vmax值降低。因此,增强心脏O2-自由基产生的情况可被视为一种能够抑制肌原纤维Ca2+-ATP酶活性的负面代谢事件。