Acute and Chronic Exposures to Nitrogen Dioxide

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Abstract
The values obtained for O2 consumption and for enzyme concentrations represent activity levels of tissue homogenate rather than whole tissue. Centrifugation at 10, 000-11,000 g removes most of the comparatively inactive structural and connective-tissue proteins with the resulting supernatant containing a relatively high concentration of mitochondrial and microsomal materials. The relative amount of this active material, based on the weight of the whole tissue, is much less in lung than in liver, kidney, or spleen. Values obtained, therefore, do not reflect relative activity of whole tissues, but rather of a distinct portion of the cellular material with the corresponding enzyme systems. Acute and chronic exposures to NO2 appear to have widespread affects on the Qo2, lacticdehydro-genase (LDH) and aldolase activity. Oxygen consumption of lung tissue was altered relatively little by either acute or chronic exposures. Exposed liver homogenate shows a marked increase over control values in acute exposures, although this tissue shows depressed values after long-term chronic exposures. The differences in Qo2 values of liver homogenate after chronic exposure are relatively small. It remains for future experiments to determine whether Qo2 values for liver homogenate from chronically exposed animals rises initially and are then depressed or if depression occurs without an initial increase. Spleen and kidney homogenates show marked increase in O2 consumption with both exposure regimens and the data give no indication of depressed activity seen with liver homogenate. O2 consumption data suggest that the enzyme systems of the tissues studied may respond differently to NO2 exposure. Lung tissue shows only a slight increase, liver tissue shows the opposite response to acute and chronic exposure, and spleen and kidney tissues show marked increases in Qo2 values. Whether these differences are due to changes in total enzyme concentrations or to other factors cannot be stated from these data. The LDH and aldolase activities are increased by both exposure regimens. The alteration of enzyme activity and O2 consumption in any organ appears to be unrelated. The relative change in activity varies widely in different organs, indicating that tissues may respond to NO2 through different mechanisms or that the effects of NO2 may not be the same for all tissues. The increase in serum values for LDH and aldolase probably indicates tissue damage with subsequent release of tissue enzyme into the blood stream. The data give no indication of the possible site of release since enzyme activities were altered in all tissues upon which measurements were made. This study was an attempt to measure some of the metabolic effects of the air pollutant NO2 on lung and other body tissues. To relate changes in O2 consumption and enzyme activities in organs to length of exposure it would be well to subject a series of animals to a single concentration of NO2 (15 ppm, for example) and study tissues from animals (exposed and control) during regular intervals after the initiation of the regimen. This would clarify the observations in oxygen consumption of liver homogenate. It would also be of value to express enzyme activity in terms of substrate utilization in order to obtain more information about the specific activity of the tissue homogenates.

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