Abstract
Summary
1. Mouse lung tissue possesses the capacity to oxidize several of the naturally occurring compounds which are capable of undergoing oxidative decomposition and giving rise to energy-yielding mechanisms. Under the limiting conditions of these exploratory experiments, the presence of a Type A, PR8 influenza virus infection in this tissue does not appear to alter, to a significant degree, these oxidative reactions. 2. Influenza infection appears to increase the capacity of host lung tissue to metabolize several compounds concerned in nucleic acid metabolism. Whether this phenomenon is indicative of cellular breakdown incidental to the viral infectious process or whether it represents an “active” degradation of specific molecules consequent to virus synthesis is still to be determined. 3. Xanthine oxidase appears to play a central role in the in vitro purine metabolism of mouse lung; the activity of this enzyme is increased in the infected tissue. The increment and decrement periods of virus proliferation roughtly parallel the increment and decrement periods of enzyme activity. In no case was a qualitative difference found between the xanthine oxidases of normal and virus infected lung tissue; the effects produced by the addition of metabolic inhibitors, the influence of methylene blue, and the end-products of the reactions were the same. The significance of these findings has been discussed.
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