Lung development in the streptozotocin rat fetus: antioxidant enzymes and survival in high oxygen.
Offspring of experimentally induced diabetic animals demonstrate delays in functional, biochemical, and morphological aspects of lung maturation, dealing mainly with the surfactant system. To investigate whether the development of the lung antioxidant enzyme system would be similarly delayed, and thus compromise their tolerance to high O2 exposure, we did the following: 1) produced the diabetic state in rats with streptozotocin injection 24 h after the onset of pregnancy; 2) examined fetal animals from streptozotocin and control rats at gestational days 19, 20, and 21, and newborn animals at day 22 for whole lung disaturated phosphatidylcholine and total phospholipid and for the three antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase; and 3) exposed newborn offspring from streptozotocin-treated and control rats to greater than 95% O2 for several days and their survival, changes in antioxidant enzymes and disaturated phosphatidylcholine and light microscopic findings in response to hyperoxic challenge were compared. Streptozotocin offspring demonstrated essentially no developmental differences in whole lung disaturated phosphatidylcholine, total phospholipid, or antioxidant enzymes activity at the 4 gestational days studied. However, newborns of streptozotocin mothers had consistently superior tolerance to hyperoxic exposure, consisting of increased survival [23/34 (68%) versus 8/26 (31%) in controls, after O2-exposure for 13 days, p less than 0.001], microscopic evidence of reduced inhibition of alveolarization (p less than 0.05), and a trend toward greater antioxidant enzymes response. Thus, in this animal model of experimental diabetes, neither the development of the antioxidant enzymes system nor the development of the surfactant system (as assessed by whole lung disaturated phosphatidylcholine and total phospholipid) appear delayed.(ABSTRACT TRUNCATED AT 250 WORDS)
D000818:Animals; D000831:Animals, Newborn; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental; D005314:Embryonic and Fetal Development / Q000187:drug effects; D005260:Female; D005325:Fetal Organ Maturity; D005865:Gestational Age; D005979:Glutathione Peroxidase / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000196:embryology* / Q000378:metabolism; D008171:Lung Diseases / Q000209:etiology*; D010088:Oxidoreductases / Q000378:metabolism*; D010100:Oxygen / Q000494:pharmacology* / Q000633:toxicity; D010713:Phosphatidylcholines / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D011247:Pregnancy; D011254:Pregnancy in Diabetics; D011650:Pulmonary Alveoli / Q000254:growth & development; D011663:Pulmonary Surfactants / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000378:metabolism
D010713:Phosphatidylcholines; D010743:Phospholipids; D011663:Pulmonary Surfactants; C017463:lecithins, disaturated; D010088:Oxidoreductases; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D010100:Oxygen