Dubick M A, Zidenberg-Cherr S, Rucker R B, Keen C L
Division of Military Trauma Research, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129.
Toxicol Lett. 1988 Aug;42(2):149-57. doi: 10.1016/0378-4274(88)90072-0.
Nutritional manganese (Mn) or copper (Cu) deficiency was investigated in Swiss-Webster mice exposed to ozone (O3). Mice rendered Mn-deficient were first reared from Mn-deficient dams and then fed a Mn-deficient (1 microgram/g) diet. Mice rendered Cu-deficient were fed a diet containing 0.2 microgram Cu/g diet. Control mice were fed a diet containing Mn at 45 micrograms/g and Cu at 8 micrograms/g. During the last week of the experiment (week 7, post-weanling), mice in each group were exposed continuously to 1.2 ppm O3 or filtered air for 7 days. Superoxide dismutase (SOD) activity in lung was then estimated. In mice breathing filtered air, neither lung Cu,Zn- nor Mn-SOD activity (U/g) was affected by diet. In O3-exposed mice, however, Mn-SOD activity was lower in the Mn-deficient group and Cu, Zn-SOD activity was lower in the Cu-deficient group. Moreover, total lung Cu,Zn-SOD activity was elevated in the Mn-deficient mice, whereas total Mn-SOD activity was elevated in the Cu-deficient mice in response to O3. These data indicate that under normal circumstances lung Cu,Zn-SOD and Mn-SOD are not affected by Cu or Mn deficiency. However, when an oxidant stress is superimposed on the Cu- or Mn-deficient condition, Cu,Zn- and Mn-SOD activities are impaired.
在暴露于臭氧（O₃）的瑞士韦伯斯特小鼠中研究了营养性锰（Mn）或铜（Cu）缺乏的情况。使小鼠缺锰的方法是，先由缺锰的母鼠饲养，然后喂食缺锰（1微克/克）的饲料。使小鼠缺铜的方法是，喂食含0.2微克铜/克的饲料。对照小鼠喂食含45微克锰/克和8微克铜/克的饲料。在实验的最后一周（第7周，断奶后），每组小鼠连续7天暴露于1.2 ppm的O₃或过滤空气中。然后估计肺中超氧化物歧化酶（SOD）的活性。在呼吸过滤空气的小鼠中，饮食对肺中铜锌超氧化物歧化酶或锰超氧化物歧化酶的活性（单位/克）均无影响。然而，在暴露于O₃的小鼠中，缺锰组的锰超氧化物歧化酶活性较低，缺铜组的铜锌超氧化物歧化酶活性较低。此外，缺锰小鼠的肺总铜锌超氧化物歧化酶活性升高，而缺铜小鼠的肺总锰超氧化物歧化酶活性因O₃而升高。这些数据表明，在正常情况下，肺中的铜锌超氧化物歧化酶和锰超氧化物歧化酶不受铜或锰缺乏的影响。然而，当在缺铜或缺锰的情况下叠加氧化应激时，铜锌超氧化物歧化酶和锰超氧化物歧化酶的活性会受损。
