Retarded development of noenatal rat lung by maternal malnutrition.
Inadequate dietary intake during late pregnancy may have significant effects on the developing fetal lung which undergoes rapid cellular multiplication and differentiation shortly before birth. The morphology, glycogen distribution and acid phosphatase activity in normal and starved neonatal rats have been studied sequentially, by using histochemical and cytochemical methods. It has been shown that the normal pattern of lung growth and enzymatic development is retarded in neonates of malnourished mothers. A slowed rate of cellular division and differentiation in the critical prenatal period resulted in a more immature air-blood barrier at birth, with glycogen retention by some epithelial cells. Delayed Type 2 cell maturation with diminished acid phosphatase activity suggests a decrease in surfactant production in the malnourished newborn. In addition, fewer alveolar macrophages with reduced acid phosphatase activity were observed in the perinatal period of starved rats; this finding might have implications for the handling of inhaled bacteria shortly after birth. These results indicate that nutritional status of the mother has a marked effect on fetal lung growth and development by inhibiting cellular proliferation, differentiation and enzyme development by epithelial and macrophagic cells.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D005260:Female; D005865:Gestational Age; D006003:Glycogen / Q000378:metabolism; D008168:Lung / Q000166:cytology / Q000196:embryology / Q000254:growth & development*; D008264:Macrophages / Q000166:cytology; D009748:Nutrition Disorders / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000166:cytology; D051381:Rats
D006003:Glycogen; D000135:Acid Phosphatase