Life Sciences, Vol. 64, No. 11, pp895-904, 1999 Scientific Problem: Characterizing the effects of dexamethasone on ODC gene expression and enzyme activity in the lung of rat pups.
Facts Pertaining the Problem: Numerous studies have shown that gestational exposure to glucocorticoid increases the productions and release of surfactant and accelerates morphological development of the fetal lung, while interruption of the pituitary-adrenal axis impairs lung growth, as do inhibitors of glucocorticoid biosynthesis. Synthetic glucocorticoids are routinely administered to pregnant women at risk of premature delivery in an attempt to accelerate the functional maturation of the fetal lung and thereby reduce the incidence of respiratory distress syndrome in the newborn, a leading cause of neonatal death in pre-term infants. Glucocorticoids did not alter surfactant production when given postnatally. However, they were found to inhibit proliferation of lung cells and to impair formation of new alveoli, suggesting that endogenous glucocorticoids may modulate cell development in the postnatal lung.
The Proposed Tentative Solution: Due to its extremely short half-life in animal tissues, ODC is rapidly induced or suppressed by agents which influence development.
The Design for the Experiment to Test the Hypothesis: Lactating CD female rats with litters of 10 pups were housed in breeding cages in a vivarium maintained at 22 degrees Celsius with a 12-h light-dark cycle, and provided food and water ad libitum. Animals were killed by decapitation and lungs and livers were quickly dissected, homogenized in 19 volumes of ice-cold 10mM Tris-HCl, centrifuged at 26,000 x g for 20 min, and the supernatant assayed for ODC activity by a modification of the method of Russell and Synder. Total liver RNA was extracted with acid guanidinium thiocyanate-phenol-choloform according to Chomczynsky and Sacchi.
The Conclusion Related to the Objectives: The results from these studies demonstrate that neonatal lung ODC activity is...