Publications
588 results found
Kelly FJ, Birch S, 1994, Pulmonary Protein Synthesis Response to Ozone, Human & Experimental Toxicology, Vol: 13, Pages: 407-410, ISSN: 0960-3271
<jats:p> 1 Exposure to either 800 or 1200 ppb ozone for 6 h did not influence the content or activity of mouse lung ribosomal RNA; in consequence pulmonary protein synthesis pathways were not altered. </jats:p><jats:p> 2 Increasing the exposure period to 24 h had a marked effect on protein metabolism which depended on the dose of ozone employed. A dose of 800 ppb resulted in a 17% increase in lung protein content. Since both lung ribosomal capacity and fractional synthesis rates were unchanged at this time, it is concluded that both a lower ribosomal activity and an increased protein degradation rate were responsible for the decrease in content. </jats:p><jats:p> 3 Exposure to 1200 ppb ozone for 24 h, paradoxically resulted in increases in both the fractional (33%) and total (19%) protein synthetic rates. These responses were due to an increased pulmonary ribosomal efficiency in the lung at this time. </jats:p><jats:p> 4 We conclude that, in the short term, reduced pulmonary synthetic capacity is not a component of ozone-induced lung injury, but rather, this important component of the repair mechanism, can be up-regulated in response to lung injury. </jats:p>
KELLY FJ, ANDREWS GA, GEORGES TM, 1994, SOLAR RADAR REVIVAL, 1992 STEP Symposium/5th COSPAR Colloquium, Publisher: PERGAMON PRESS LTD, Pages: 147-150
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- Citations: 1
DIMARCO SF, KELLY FJ, CHILDRESS EF, et al., 1994, FIELD COMPARISON OF 2 DIRECTIONAL WAVE GAUGES, Conference on Challenges and Opportunities in the Marine Environment (MTS 94), Publisher: MARINE TECHNOLOGY SOC, Pages: 32-38
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HUNT AN, KELLY FJ, POSTLE AD, 1994, EFFECTS OF STARVATION AND THYROID-HORMONES ON THE COMPOSITIONS OF LUNG PHOSPHATIDYLCHOLINE MOLECULAR-SPECIES IN THE GUINEA-PIG, 4th International Symposium on Lung Surfactant, Publisher: KARGER, Pages: 96-100
CHEESEMAN KH, HOLLEY A, KELLY FJ, et al., 1993, BIOAVAILABILITY OF RRR-ALPHA-TOCOPHEROL ESTERS IN MAN, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: 488-488, ISSN: 0891-5849
Town GI, Phillips GJ, Landreau M, et al., 1993, Dexamethasone treatment fails to reduce oxygen-induced lung injury in the preterm guinea pig, Biochemical Pharmacology, Vol: 46, Pages: 1565-1572, ISSN: 0006-2952
KELLY FJ, WASIL M, CHEESEMAN K, et al., 1993, LUNG RRR-A-TOCOPHEROL KINETICS IN PRETERM GUINEA-PIGS DURING OXIDATIVE STRESS, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: 489-489, ISSN: 0891-5849
Kelly FJ, Cheeseman KH, 1993, Distribution of vitamin e between tissues during periods of hyperoxic and nutritional stress in the preterm guinea pig, Comparative Biochemistry and Physiology Part A: Physiology, Vol: 105, Pages: 549-554, ISSN: 0300-9629
Kelly FJ, Birch S, 1993, Ozone exposure inhibits cardiac protein synthesis in the mouse, Free Radical Biology and Medicine, Vol: 14, Pages: 443-446, ISSN: 0891-5849
Kelly FJ, 1993, Glutathione content of the small intestine: regulation and function, British Journal of Nutrition, Vol: 69, Pages: 589-595, ISSN: 0007-1145
<jats:p>In ad lib.-fed rats the epithelium of the small intestine, like the liver, contains large quantities of glutathione, 17.0 and 32.4 nmol/mg protein respectively. Following 24 h food restriction the glutathione content in both tissues fell 53 and 69% respectively. Unlike the liver, however, the glutathione content of the intestinal mucosa is not regulated to a diurnal rhythm, suggesting that the liver may provide glutathione or glutathione precursors to maintain intestinal glutathione levels. Intestinal epithelial cell preparations obtained from 24 h food-deprived rats had depleted glutathione stores (50%) and as a consequence were more susceptible to the oxidizing effects of cumene hydroperoxide. These results suggest that if glutathione plays a major role in the defence of the intestinal mucosa from ingested toxins then depletion of this defence during periods of food restriction could significantly increase the susceptibility of the individual to toxins present in the diet.</jats:p>
Langley SC, Brown RK, Kelly FJ, 1993, Reduced Free-Radical-Trapping Capacity and Altered Plasma Antioxidant Status in Cystict Fibrosis, Pediatric Research, Vol: 33, Pages: 247-250, ISSN: 0031-3998
Burdge GC, Kelly FJ, Postle AD, 1993, Mechanisms of hepatic phosphatidylcholine synthesis in the developing guinea pig: contributions of acyl remodelling and of <i>N</i>-methylation of phosphatidylethanolamine, Biochemical Journal, Vol: 290, Pages: 67-73, ISSN: 0264-6021
<jats:p>Hepatic phosphatidylcholine (PC) from the immature fetal guinea pig at day 55 of gestation comprised mainly unsaturated molecular species containing C18:2(n-6) and C22:6(n-3) at the sn-2 position, reflecting placental permeability to essential fatty acids. At both day 55 and term (day 68), [Me-14C]choline was incorporated in utero over 3 h largely into sn-1-C16:0 PC species, with incorporation into sn-1-C18:0 PC species increasing by 18 h of incubation. Comparison of specific radioactivities after 3 h and 18 h suggests PC acyl remodelling by phospholipase A1. No incorporation into C20:4(n-6)-containing PC species could be detected of either [Me-14C]choline in vivo or CDP-[Me-14C]choline in isolated microsomes. The major phosphatidylethanolamine (PE) species were 16:0/22:6 and 18:0/22:6. Although [14C]ethanolamine was initially incorporated mainly into sn-1-C16:0 species, specific-radioactivity analysis suggested differential turnover rather than acyl remodelling. [1,2-14C]Ethanolamine and [Me-14C]methionine incorporation into PC molecular species indicated that both newly synthesized and total PE pools were available for N-methylation. Since the PC pool synthesized from PE included C20:4- and C22:6-containing species, N-methylation may provide a mechanism for supplying essential long-chain fatty acids to developing tissues that can be regulated independently from bulk PC synthesis.</jats:p>
Burdge GC, Kelly FJ, Postle AD, 1993, Synthesis of phosphatidylcholine in guinea-pig fetal lung involves acyl remodelling and differential turnover of individual molecular species, Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol: 1166, Pages: 251-257, ISSN: 0005-2760
Langley SC, Kelly FJ, 1993, N-acetylcysteine ameliorates hyperoxic lung injury in the preterm guinea pig, Biochemical Pharmacology, Vol: 45, Pages: 841-846, ISSN: 0006-2952
Town IG, Phillips GJ, Murdoch E, et al., 1993, Temporal Association Between Pulmonary Inflammation and Antioxidant Induction Following Hyperoxic Exposure of the Preterm Guinea Pig, Free Radical Research Communications, Vol: 18, Pages: 211-221, ISSN: 8755-0199
Kelly FJ, 1993, Free radical disorders of preterm infants, British Medical Bulletin, Vol: 49, Pages: 668-678, ISSN: 0007-1420
Langley SC, Rickett GW, Hunt A, et al., 1993, Effects of the glucocorticoid agonist, RU28362, and the antagonist RU486 on lung phosphatidylcholine and antioxidant enzyme development in the genetically obese Zucker rat, Biochem Pharmacol, Vol: 45, Pages: 543-551, ISSN: 0006-2952
The biochemical maturation of the lung in late gestation and in the young animal is regulated by glucocorticoids. The present study was aimed at dissociating the different glucocorticoid receptor sites involved in these regulatory functions. The obese Zucker rat was selected as a model for this study as it exhibits hypersensitivity to glucocorticoid hormone action by virtue of its elevated receptor numbers and activity. Two synthetic steroid analogues were administered to obese animals; RU28362, a specific type II receptor agonist, and the type II antagonist RU486. RU28362 promoted a strong catabolic effect, which was associated with reduced food intake and the abolition of growth in the rats. The agonist, RU28362, attenuated developmental increases in antioxidant enzyme activities, and altered the growth of the tissue. At the age studied, development of the lung phosphatidylcholine (PC) system was almost complete, but RU28362 increased disaturated PC 16:0/16:0 concentrations by almost 2-fold, and altered the molecular composition of total pulmonary PC. RU486 attenuated the growth of the rats and reduced their food intake. Treatment with the type II antagonist attenuated lung growth and increased the activities of pulmonary copper zinc (Cu/Zn) and manganese (Mn) superoxide dismutases. RU486 had no effect on lung PC concentrations and molecular composition. The data suggest a role for type I glucocorticoid receptors in the regulation of the antioxidant enzyme system in the lung, as type II antagonism will channel endogenous glucocorticoid binding to the type I site. Type II receptor binding would appear to play a role in regulating the lung PC content.
Langley SC, Phillips GJ, Tahedl S, et al., 1992, Dietary supplementation of vitamin E fails to prevent the development of hyperoxic lung injury in the premature guinea pig, Comparative Biochemistry and Physiology Part A: Physiology, Vol: 103, Pages: 793-799, ISSN: 0300-9629
KELLY FJ, 1992, NUTRIENT SUPPLY REGULATES LEFT-VENTRICULAR GROWTH IN THE IMMATURE HEART AT THE SITE OF PEPTIDE-CHAIN INITIATION, Publisher: AMER HEART ASSOC, Pages: 843-843, ISSN: 0009-7322
Langley SC, Kelly FJ, 1992, Differing response of the glutathione system to fasting in neonatal and adult guinea pigs, Biochemical Pharmacology, Vol: 44, Pages: 1489-1494, ISSN: 0006-2952
Langley SC, Kelly FJ, 1992, Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig, American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol: 263, Pages: L357-L362, ISSN: 1040-0605
<jats:p> Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses. </jats:p>
LANGLEY SC, KELLY FJ, 1992, EFFECT OF FOOD RESTRICTION ON HYPEROXIA-INDUCED LUNG INJURY IN PRETERM GUINEA-PIG, AMERICAN JOURNAL OF PHYSIOLOGY, Vol: 263, Pages: L357-L362, ISSN: 0002-9513
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- Citations: 12
BURDGE GC, KELLY FJ, POSTLE AD, 1992, Mechanisms of synthesis of polyunsaturated phosphatidylcholine molecular species by guinea pig liver, Biochemical Society Transactions, Vol: 20, Pages: 299S-299S, ISSN: 0300-5127
Kelly FJ, Safavi M, Cheeseman KH, 1992, Tissue α-tocopherol status during late fetal and early neonatal life of the guinea-pig, British Journal of Nutrition, Vol: 67, Pages: 457-462, ISSN: 0007-1145
<jats:p>The α-tocopherol content of a number of different fetal, neonatal and maternal guinea-pig tissues was determined and compared with plasma and erythrocyte α-tocopherol values. During late gestation, the fetal liver appears to act as a storage site for α-tocopherol, the majority of which is released immediately following birth. In contrast, lung and brain vitamin E levels are relatively constant over the final period of gestation and during early neonatal life. The ontogeny of α-tocopherol in brain and lung was similar to that for erythrocytes while plasma α-tocopherol content varied considerably and did not accurately reflect tissue α-tocopherol status. Surprisingly, fetal and maternal lung α-tocopherol concentrations were similar at all time-points considered, whereas fetal liver α-tocopherol status was always considerably greater than maternal liver α-tocopherol content. These results, if representative of the human fetus, suggest that preterm infants may not have tissue α-tocopherol concentrations as low as previously assumed and that during the perinatal period erythrocyte α-tocopherol content is a more accurate indicator of tissue α-tocopherol concentration than plasma α-tocopherol content.</jats:p>
Fussell JC, Kelly FJ, 1992, Characterization of a cell-free protein synthesizing system from rat lung, International Journal of Biochemistry, Vol: 24, Pages: 703-706, ISSN: 0020-711X
Ashton MR, Postle AD, Hall MA, et al., 1992, Phosphatidylcholine composition of endotracheal tube aspirates of neonates and subsequent respiratory disease., Archives of Disease in Childhood, Vol: 67, Pages: 378-382, ISSN: 0003-9888
Kelly FJ, Fussell JC, Postle TD, 1992, Effect of acute food restriction on pulmonary growth and protein turnover in preterm guinea pigs, American Journal of Physiology-Endocrinology and Metabolism, Vol: 262, Pages: E240-E245, ISSN: 0193-1849
<jats:p> The effects of food restriction on the growth and protein turnover of the immature lung were investigated. Preterm guinea pigs, delivered by cesarean section at 65 days gestation (term = 68 days), were given free access to a lactating dam or restricted from feeding for 48 h. Food restriction resulted in significantly reduced body and lung (P less than 0.05) weight compared with fed controls. The rate of pulmonary protein synthesis determined in vivo was reduced by 33% in the food-restricted pups (28.9 +/- 10.2 vs. 19.4 +/- 4.5%, P less than 0.05 for control and food-restricted pups, respectively), whereas the calculated rate of protein breakdown remained unchanged. The inhibition of protein synthesis was accounted for by a 36% decrease in ribosomal efficiency (11.03 +/- 2.61 vs. 7.04 +/- 1.26%, P less than 0.01 for control and food-restricted pups, respectively), whereas ribosomal capacity was unaltered. Polyribosomal analysis indicated an increase in the proportion of RNA present in polysomes and a fall in the free monomer pool (26%), suggesting that food restriction blocked translation by reducing the rate of peptide chain elongation. This finding was confirmed by the analysis of ribosome transit times, which indicated a significant increase in the elongation rate in the lungs from food-restricted pups (0.51 +/- 0.11 vs. 0.94 +/- 0.19 min, P less than 0.05 for control and food-restricted pups, respectively). These results imply that nutrient supply plays an important role in protein deposition and hence growth and repair capacity of the immature lung. </jats:p>
KELLY FJ, FUSSELL JC, POSTLE TD, 1992, EFFECT OF ACUTE FOOD RESTRICTION ON PULMONARY GROWTH AND PROTEIN-TURNOVER IN PRETERM GUINEA-PIGS, AMERICAN JOURNAL OF PHYSIOLOGY, Vol: 262, Pages: E240-E245, ISSN: 0002-9513
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Kelly FJ, Rickett GWM, Phillips GJ, 1992, Magnitude of Hyperoxic Stress and Degree of Lung Maturity Determine the Nature of Pulmonary Antioxidant Response in the Guinea Pig, Free Radical Research Communications, Vol: 17, Pages: 335-347, ISSN: 8755-0199
McElroy MC, Postle AD, Kelly FJ, 1992, Catalase, superoxide dismutase and glutathione peroxidase activities of lung and liver during human development, Biochim Biophys Acta, Vol: 1117, Pages: 153-158, ISSN: 0006-3002
The developmental expression of catalase, superoxide dismutase (both Mn-SOD and Cu/Zn-SOD) and glutathione peroxide activities were determined in human lung and liver from 10 wk gestation to 3 months following birth. Pulmonary superoxide dismutase and glutathione peroxidase activities did not change appreciably over this period. Catalase activity however, increased from 20.9 +/- 7.8 U/mg protein (n = 29) at 11-20 wk gestation to 73 +/- 27.5 U/mg protein (n = 30; P less than 0.001) following normal delivery (41-60 wk post-conceptual age). Lung catalase activity was temporally associated with the late gestational increase in the fractional content of lung DPPC (r = 0.79, P less than 0.01). In contrast with the lung, liver total superoxide dismutase activity increased from 2.5 +/- 0.6 U/mg protein (n = 27) between 11 and 20 wk gestation to 9.4 +/- 4.4 U/mg protein after term (n = 22; P less than 0.001). Since hepatic Mn-superoxide dismutase activity did not change over this period, the increase was attributed to elevated expression of Cu/Zn-superoxide dismutase. Liver glutathione peroxidase activities remained relatively constant during the same period, while hepatic catalase activity, although constant during gestation (60 +/- 15.6 microU/mg protein), increased significantly following birth (99.7 +/- 33.0 microU/mg protein; P less than 0.001). These results demonstrate that the developmental expression of antioxidant enzymes differs between tissues and that, unlike many commonly used laboratory species, only increased expression of catalase activity is associated with human lung development.
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