11-BETA-HYDROXYSTEROID DEHYDROGENASE OF RAT LUNG - ENZYME-KINETIC, OXIDASE-REDUCTASE RATIO, ELECTROLYTE AND TRACE-ELEMENT DEPENDENCE

The modulation of the intracellular glucocorticoidal effect on surfact ant synthesis of the fetal lung by the metabolic capacity of 11 beta-h ydroxysteroid dehydrogenase (11 beta-HSD) could be an important factor in lung maturation. The kinetic properties of microsomal 11 beta-HSD of the rat lung are characterized with respect to product inhibition, substrate specificity, effect of electrolytes or trace elements, and t he dependence of the oxidase reductase (OR) ratio on incubation condit ions. With NADP(+) product inhibition of the reductase was demonstrate d. The most common trace elements and electrolytes exhibited no effect on the activity of 11 beta-HSD. It is shown that the OR ratio was str ongly dependent on assay conditions. With optimal assay conditions oxi dase activity exceeds reductase activity in adult and fetal rat lung m icrosomes (OR ratio >1). Thus, glucocorticoids are mainly metabolized to their inactive forms. The enzyme activity in the adult is about 10 times higher than in the fetal lung. The low enzyme activity in fetal lungs could be the reason why the glucocorticoidal effects on surfacta nt synthesis are not suppressed despite the predominance of oxidase ac tivity.