Kelly F J, Birch S
Cardiovascular Research, Rayne Institute, St. Thomas's Hospital, London, England.
Free Radic Biol Med. 1993 Apr;14(4):443-6. doi: 10.1016/0891-5849(93)90094-b.
Ozone is a major environmental oxidant pollutant. Following ozone inhalation, there are a number of marked pulmonary responses depending on the extent and duration of exposure. Recently it has been established that ozone exposure may also result in cardiac injury. In this study we show that exposure of mice to 800 ppb ozone for as little as 6 h results in a 16% decrease in cardiac protein synthesis rates (p < .02). The fall in protein synthesis is due primarily to a reduced rate of ribosomal efficiency (40%) in the hearts of ozone-exposed mice. This change in cardiac protein metabolism is accompanied by increased levels of two markers of tissue injury: edema and protein carbonyl content. It is unlikely, however, that these observations represent a direct action of ozone on the heart, but rather an indirect effect, possibly mediated by lipid peroxidation products generated in the lung.
臭氧是一种主要的环境氧化性污染物。吸入臭氧后，根据接触的程度和持续时间会出现许多明显的肺部反应。最近已证实，接触臭氧也可能导致心脏损伤。在本研究中，我们表明，将小鼠暴露于800 ppb的臭氧中，即使仅6小时，心脏蛋白质合成率也会降低16%（p <.02）。蛋白质合成的下降主要是由于臭氧暴露小鼠心脏中核糖体效率降低了40%。心脏蛋白质代谢的这种变化伴随着两种组织损伤标志物水平的升高：水肿和蛋白质羰基含量。然而，这些观察结果不太可能代表臭氧对心脏的直接作用，而更可能是一种间接效应，可能由肺中产生的脂质过氧化产物介导。
