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Biomedical subjects

A P Autor

Publications and source records attributed to A P Autor.

At least 37 records · Page 2Linked to original sources
PubMed1980

Proposed mechanism for neonatal rat tolerance to normobaric hyperoxia.

Induction of two forms of superoxide dismutase, catalase and glutathione peroxidase, occurs very rapidly in neonatal rat lung tissue upon exposure of these animals to 94 + % normobaric oxygen. No such oxygen-mediated enzyme induction occurs in the lungs of adult rats. The aged-dependent pattern of enzyme induction correlates with the well-established age-dependent tolerance of neonatal rats to hyperoxia. Enzyme induction occurs in the lungs of neonates in only those species known to be resistant to oxygen-provoked lung damage. Compromise of oxygen-mediated enzyme induction predisposed the neonatal rats to pulmonary oxygen toxicity. These data have formed the basis of the proposal that oxygen induction of the superoxide dismutases catalase and glutathione peroxidase provides a vital part of the defense mechanism against oxygen toxicity. A biochemical mechanism of oxygen-provoked pulmonary damage has been elaborated to explain the role of each enzyme in the protection against oxygen and free radical toxicity.

Age Factors↗
PubMed1979

Phospholipid-dependence of oestrone UDP-glucuronyltransferase and p-nitrophenol UDP-glucuronyltransferase.

Hepatic UDP-glucuronyltransferase activity was resolved into two fractions, one exhibiting oestrone glucuronyltransferase activity and the other exhibiting p-nitrophenol glucuronyltransferase activity. Hydroxyapatite-column chromatography removed greater than 95% of the phospholipids from both preparations. The partially purified delipidated enzymes were essentially devoid of catalytic activity, but activities were restored by the addition of phospholipids or phosphatidylcholine mixtures containing various saturated and unsaturated fatty acids. Both oestrone and p-nitrophenol glucuronyl-transferase activities were reconstituted to similar degrees with the phosphatidylcholine mixtures. When purified phospholipids were tested, phosphatidylcholine and lysophosphatidylcholine were most effective in restoring activity, whereas phosphatidylethanolamine was the least effective. These results further suggest that oestrone and p-nitrophenol UDP-glucuronyltransferases are dependent on phospholipids for their activity.

Animals↗
PubMed1978

Relationship between fatty acids and lipid peroxidation in lungs of neonates.

Triglycerides from the lungs of neonatal rats and mice were found to contain large amounts of the polyunsaturated fatty acids, arachidonate (20:4) and docosahexaeonoate (22:6). These fatty acids were diminished or absent in the triglycerides from the lungs of adult rats and mice and both neonatal and adult guinea pigs. No age-related changes were observed in the fatty acid composition of lung phospholipids in any of these species. The presence of arachidonic acid and docosahexaenoic acid in lung triglycerides correlated with the ability of these lungs to peroxidize lipids in vitro in all species. Depletion of lung triglycerides in neonatal rats by fasting abolished this lipid peroxidizing activity.

Age Factors↗
PubMed1977

Oxygen therapy and hyaline membrane disease: the effect of hyperoxia on pulmonary superoxide dismutase activity and the mediating role of plasma or serum.

In vitro and in vivo hyperoxic exposure of the lungs of normal immature animals resulted in a rapid increase of pulmonary superoxide dismutase activity. The increase of pulmonary SOD activity with in vitro hyperoxic exposure requires the presence of plasma or serum in the incubation medium. Twenty-three out of 26 plasma samples from premature infants without hyaline membrane disease were found to support the hyperoxic increaase of pulmonary SOD activity, whereas only five of 15 plasma samples from infants with HMD were effective. A defective plasma-lung interaction in infants with HMD may result in an inability to increase pulmonary levels of this presumed protective enzyme during hyperoxic therapy.

Animals↗
PubMed1976

Developmental characteristics of pulmonary superoxide dismutase: relationship to idiopathic respiratory distress syndrome.

Pulmonary superoxide dismutase (SOD) acitivity was determined for various groups of human fetuses, infants, and adults. Enzyme activity was found to increase with age from a low of 17 +/- 1 units/mg DNA in fetal lung to 49 +/- 6 units/mg DNA in infant lung and finally to 110.2 +/- 14.8 units/mg DNA in adult lung (P less than 0.05). No difference in lung SOD activity was demonstrated between normal infants and those with idiopathic respiratory distress/hyaline membrane disease (IRDS/HMD). No significant differences in SOD activity were found among all the samples of infant blood. Adult blood samples, however, contained significantly greater SOD activity both in terms of heme concentration and volume of whole blood (P less than 0.05). SOD activity in lung tissue from both rats and rabbits were also found to increase with age from a low value in fetal animals to a maximum activity in adults (P less than 0.05). Exposure of New Zealand White rabbits, prematurely delivered by caesarian section, to 80% oxygen for 24 hr resulted in a 42% increase in lung SOD activity. Similarly, 7-day-old Sprague-Dawley rats exposed to 85% oxygen for 24 hr showed a 43% increase in pulmonary SOD activity. No increase in pulmonary SOD was observed when adult rats were exposed to 85% oxygen for 24 hr. The effect of hyperoxia on SOD activity in excised lung was investigated. Rat lung, incubated in either heparinized whole blood or in plasma and exposed to 100% oxygen, showed a 30% increase in SOD activity after 2 hr. This capacity of lung tissue to respond to hyperoxia in vitro with increased SOD activity was age dependent. The maximum increase in SOD activity was seen with lungs from 10-12-day-old rats. The oxygen-stimulated increase in lung SOD activity disappeared at about 19-20 days of age.

Adult↗