McDonough K H, Henry J J, Spitzer J J
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Biochim Biophys Acta. 1987 Nov 6;926(2):127-31. doi: 10.1016/0304-4165(87)90228-5.
Freshly isolated adult rat heart cells were used to study the effects of oxygen-free radicals on the myocardial oxidation of different substrates. The calcium-tolerant quiescent cells were incubated with xanthine plus xanthine oxidase as the source of free radicals. The oxidation of exogenous glucose, lactate and octanoate was severely inhibited (approx. 70%) by products of xanthine oxidase activity. Superoxide dismutase plus catalase effectively prevented the inhibition of oxidation. Cellular high energy phosphate levels were decreased in the presence of the oxygen free radical generating system although cell viability determined by Trypan blue exclusion and light microscopic assessment of normal morphology was not affected. These data suggest that oxygen free radicals decrease myocardial substrate oxidation which may contribute to the functional and ultrastructural changes in the myocardium under conditions such as reoxygenation after hypoxia and reperfusion after ischemia.
新鲜分离的成年大鼠心脏细胞被用于研究氧自由基对不同底物心肌氧化的影响。将耐钙的静止细胞与作为自由基来源的黄嘌呤加黄嘌呤氧化酶一起孵育。黄嘌呤氧化酶活性产物严重抑制了外源性葡萄糖、乳酸和辛酸的氧化（约70%）。超氧化物歧化酶加过氧化氢酶可有效防止氧化抑制。尽管通过台盼蓝排斥法测定的细胞活力和正常形态的光学显微镜评估未受影响，但在氧自由基生成系统存在的情况下，细胞高能磷酸水平降低。这些数据表明，氧自由基会降低心肌底物氧化，这可能导致在诸如缺氧后复氧和缺血后再灌注等情况下心肌的功能和超微结构变化。
