Lung specimens were obtained from 9 patients with shock lung (adult respiratory distress syndrome), immediately after death, and from 8 controls. They were analysed for phospholipid content anf for fatty acid composition of sphingomyelin and lecithin. We found an elevated phospholipid content in the affected lungs but a decreased dipalmitoyllecithin fraction of total lecithin as indicated by 127% elevated content of oleic acid in lecithin. As a consequence the relation between the palmitic acid and oleic acid moiety of lecithin shifted from 2.32 in the normal lungs to 1.64 in the diseased lungs. Since the content of dipalmitoyllecithin is closely related to the function of the surfactant system we conclude, that the alteration of surfactant function, observed in patients with adult respiratory distress syndrome may be at least in part a result of an altered surfactant metabolism, but we cannot rule out, that the findings represent an epiphenomenon in shock lung.

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Epoxide hydratase activity with benzo[a]pyrene 4,5-oxide and glutathione S-transferase activity with 2,4-dinitrochlorobenzene as substrates were determined in cultured fibroblasts from skin biopsies of different donors and from several biopsies of the same donor. Variation of the results from experiment to experiment was reduced by the use of a reference cell strain and expression of the results as activities relative to those of the reference cells. Epoxide hydratase activity varied 2.3-fold in 39 cultures from the same subject (the variation coefficients were 0.22 and 0.15, respectively). The results indicate that, at least in skin fibroblasts, genetically caused interindividual differences in epoxide hydratase activities do not exist or are negligibly small or very rare. Glutathione S-transferase activity varied more in cultures from different donors (variation coefficient = 0.22) than in different cultures from the same donor (variation coefficient = 0.08), but the highest and the lowest activities only differed by a factor of 2.3. No significant differences in either enzyme activity were observed between males, females, subjects without tumours, lung carcinoma bearers and melanoma patients.

Retinoids are known to inhibit the substrate mediated enzyme induction of benzo[a]pyrene metabolizing enzymes. Consequently, the effect of two retinoids on the induction of benzo[a]pyrene metabolizing enzymes by the more potent inductor 2,3,7,8-tetrachlorodibenzo-p-dioxine (TCDD) was investigated. The studies were performed with human diploid fibroblasts in culture. Vitamin A palmitate and all-trans-retinoic-acid were found to prevent the TCDD induced increase of benzo[a]pyrene metabolism in a dose-dependent manner. The fact that this effect was immediately reversible makes it unlikely that it was due to non-specific toxic effects. The data suggest that retinoids cause a preferential inhibition of the de novo synthesis of benzo[a]pyrene metabolizing enzymes.