1 Exposure to either 800 or 1200 ppb ozone for 6 h did not influence the content or activity of mouse lung ribosomal RNA; in consequence pulmonary protein synthesis pathways were not altered.
2 Increasing the exposure period to 24 h had a marked effect on protein metabolism which depended on the dose of ozone employed. A dose of 800 ppb resulted in a 17% increase in lung protein content. Since both lung ribosomal capacity and fractional synthesis rates were unchanged at this time, it is concluded that both a lower ribosomal activity and an increased protein degradation rate were responsible for the decrease in content.
3 Exposure to 1200 ppb ozone for 24 h, paradoxically resulted in increases in both the fractional (33%) and total (19%) protein synthetic rates. These responses were due to an increased pulmonary ribosomal efficiency in the lung at this time.
4 We conclude that, in the short term, reduced pulmonary synthetic capacity is not a component of ozone-induced lung injury, but rather, this important component of the repair mechanism, can be up-regulated in response to lung injury.