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Updated: Aug 14, 2026
Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Superoxide dismutase activity in lung from copper- and manganese-deficient mice exposed to ozone
M A Dubick1, S Zidenberg-Cherr, R B Rucker
1Division of Military Trauma Research, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129.
Abstract:
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.
Insights
Nutrient deficiencies in manganese (Mn) or copper (Cu) impair lung enzyme activity when mice are exposed to ozone (O3) oxidant stress. These findings highlight the critical role of essential minerals in mitigating environmental respiratory damage.
Area of Science:
- Environmental Toxicology
- Nutritional Biochemistry
- Respiratory Physiology
Background:
- Ozone (O3) is a significant air pollutant causing oxidative stress in the lungs.
- Essential trace minerals like manganese (Mn) and copper (Cu) are crucial for antioxidant enzyme function.
- The interplay between nutritional status and environmental oxidant exposure on lung defense mechanisms is not fully understood.
Purpose of the Study:
- To investigate the impact of nutritional manganese (Mn) or copper (Cu) deficiency on lung superoxide dismutase (SOD) activity in mice exposed to ozone (O3).
- To determine if pre-existing mineral deficiencies exacerbate the effects of O3-induced oxidative stress on lung antioxidant enzymes.
Main Methods:
- Swiss-Webster mice were fed diets deficient in either Mn or Cu, or adequate control diets.
- Mice were exposed to 1.2 ppm O3 or filtered air for 7 days during the final week of the experiment.
- Superoxide dismutase (SOD) activity, specifically Cu,Zn-SOD and Mn-SOD, was measured in lung tissue.
Main Results:
- In mice breathing filtered air, neither Mn nor Cu deficiency affected lung Cu,Zn-SOD or Mn-SOD activity.
- Ozone exposure led to reduced Mn-SOD activity in Mn-deficient mice and reduced Cu,Zn-SOD activity in Cu-deficient mice.
- Ozone exposure resulted in elevated total lung Cu,Zn-SOD activity in Mn-deficient mice and elevated total Mn-SOD activity in Cu-deficient mice.
Conclusions:
- Under normal conditions, lung Cu,Zn-SOD and Mn-SOD are not significantly affected by Cu or Mn deficiency alone.
- When exposed to an oxidant stressor like O3, pre-existing Cu or Mn deficiencies impair the normal regulation of Cu,Zn-SOD and Mn-SOD activities.
- These findings underscore the importance of adequate mineral intake for maintaining lung antioxidant defenses against environmental pollutants.
