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Toxicol Lett. 1988 Aug;42(2):149-57.

Superoxide dismutase activity in lung from copper- and manganese-deficient mice exposed to ozone.

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Division of Military Trauma Research, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129.


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.

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