Maternal copper supplementation protects the neonatal rat lung against the adverse effects of maternal nicotine exposure

2000 ◽  
Vol 12 (2) ◽  
pp. 97 ◽  
Author(s):  
G. S. Maritz ◽  
H. L. Matthews ◽  
J. Aalbers
Keyword(s):  
Adverse Effects ◽  
Lung Development ◽  
Lysyl Oxidase ◽  
Neonatal Rat ◽  
Control Group ◽  
Nicotine Exposure ◽  
Rat Lung ◽  
Alveolar Volume ◽  
Copper Supplementation ◽  
Neonatal Lung

Maternal nicotine exposure interferes with the extracellular formation of the connective tissue frame-work of the neonatal lung, a process that is dependent on copper-dependent lysyl oxidase. It has been shown that, during the phase of lung development associated with alveolarization, maternal nicotine exposure resulted in a reduction in the copper content and thus conceivably in the activity of lysyl oxidase of the neonatal lung. Therefore the aims of this study were (a) to determine the effects of maternal nicotine exposure during gestation and lactation on neonatal lung development, and (b) to establish whether maternal copper supplementation during gestation and lactation prevented the effect of maternal nicotine exposure on neonatal lung development. Pregnant rats were randomly divided into four groups: the control group received saline; the second group received 1 mg nicotine (kg bodyweight)–1 day–1 subcutaneously; the third group received 1 mg copper (kg bodyweight)–1 day–1; and the fourth group received both nicotine and copper in the same quantities as the previous two groups. Lung tissue of 14- and 42-day-old rat pups were processed for light microscopy. Maternal nicotine exposure during gestation and lactation resulted in (a) decreased alveolar number, (b) reduced internal surface area and (c) increased alveolar volume. Copper supplementation during gestation and lactation prevented the adverse effects of maternal nicotine exposure during gestation and lactation on the development of the alveolar region of the rat lung.

scholarly journals Postnatal development of rat lung. Changes in lung lectin, elastin, acetylcholinesterase and other enzymes

1980 ◽  
Vol 188 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Janet T. Powell ◽  
Philip L. Whitney
Keyword(s):  
Lung Development ◽  
Specific Activity ◽  
Neonatal Rat ◽  
Cholinergic Innervation ◽  
Morphological Evidence ◽  
Rat Lung ◽  
Lectin Activity ◽  
Respiratory Organ ◽  
Morphometric Methods ◽  
Glucose 6 Phosphate Dehydrogenase

The development of rat lung from a primitive gas-exchange organ to the mature respiratory organ is in large part a postnatal phenomenon that has been well characterized by morphological and morphometric methods. The alveolarization of the lung is achieved during the first 3 weeks of life. Cholinergic innervation of rat lung also appears postnatally. We have monitored the presence or activity of several proteins during postnatal rat lung development. Newborn-rat lung contains negligible amounts of acetylcholinesterase, but the specific activity of acetylcholinesterase reaches adult values by postnatal day 10–11. Neonatal-rat lung does not contain significant amounts of β-galactoside-binding protein [Powell (1980) Biochem. J.187, 123–129]. The activity of this endogenous lung lectin was apparent at about day 6, was maximal between days 10 and 13 before declining 8–10-fold to reach adult values. Elastin has been implicated from morphological evidence as critical to lung restructuring. We have quantified the amount of desmosine and isodesmosine per g wet wt. of lung. The concentration of elastin, by this criterion, was low and stationary until postnatal day 7; a dramatic increase in elastin concentration occurred between days 10 and 20, when adult values were reached. The peak of lung-lectin activity was coincident with the maturation of acetylcholinesterase and the beginning of rapid elastin cross-linking. The specific activities of angiotensin-converting enzyme, carbonic anhydrase, choline kinase and glucose 6-phosphate dehydrogenase were also monitored.

Biomedical response of neonatal rat lung to maternal nicotine exposure

1995 ◽  
Vol 2 (1) ◽  
pp. 47-54 ◽  
Author(s):  
G.S. Maritz ◽  
K. Najaar
Keyword(s):  
Neonatal Rat ◽  
Nicotine Exposure ◽  
Rat Lung

FGF-18 is upregulated in the postnatal rat lung and enhances elastogenesis in myofibroblasts

2005 ◽  
Vol 288 (1) ◽  
pp. L43-L51 ◽  
Author(s):  
Bernadette Chailley-Heu ◽  
Olivier Boucherat ◽  
Anne-Marie Barlier-Mur ◽  
Jacques R. Bourbon
Keyword(s):  
Lung Development ◽  
Lysyl Oxidase ◽  
Smooth Muscle Actin ◽  
Fold Increase ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Rat Lung ◽  
Fetal Fibroblasts

The fibroblast growth factors (FGFs) are key players in fetal lung development, but little is known about their status in postnatal lung. Here, we investigated the expression pattern of FGF-18 transcripts through the perinatal period and evidenced a sevenfold increase after birth that paralleled changes in elastin expression. In vitro, recombinant human (rh)FGF-18 had a mitogenic activity on day 21 fetal rat lung fibroblasts and stimulated its own expression in the latter, whereas FGF-2 inhibited it. At 50 or 100 ng/ml, rhFGF-18 increased the expression of α-smooth muscle actin (α-SMA; 2.5-fold), a characteristic marker of myofibroblasts, of tropoelastin (6.5-fold), of lysyl oxidase (2-fold), and of fibulins 1 and 5 (8- and 2.2-fold) in confluent fibroblasts isolated from fetal day 21 lung; similar results were obtained with fibroblasts from day 3 postnatal lungs. Elastin protein expression was also slightly increased in fetal fibroblasts. Lung analysis on day 4 in rat pups that had received rhFGF-18 (3 μg) on days 0 and 1 showed a 1.7-fold increase of tropoelastin transcripts, whereas α-SMA transcripts were unchanged. In contrast, rhFGF-2 markedly decreased expression of elastin in vitro and in vivo and of fibulin 5 in vitro. In addition, vitamin A, which is known to enhance alveolar development, elevated FGF-18 and elastin expressions in day 2 lungs, thus advancing the biological increase. We postulate that FGF-18 is involved in postnatal lung development through stimulating myofibroblast proliferation and differentiation.

Constitutive endothelial nitric oxide synthase gene expression is regulated during lung development

1995 ◽  
Vol 268 (4) ◽  
pp. L589-L595 ◽  
Author(s):  
N. Kawai ◽  
D. B. Bloch ◽  
G. Filippov ◽  
D. Rabkina ◽  
H. C. Suen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Lung Development ◽  
Blot Hybridization ◽  
Neonatal Rat ◽  
Mrna Levels ◽  
Rat Lung

Nitric oxide (NO), a potent vasodilator, is a free-radical gas synthesized from L-arginine by nitric oxide synthases (NOS). NO appears to have an important role in perinatal changes in pulmonary vascular resistance. We previously identified mRNA encoding the constitutive endothelial NOS (ceNOS) isoform in human pulmonary tissue. To begin investigating functions of this enzyme in perinatal pulmonary development, we measured ceNOS mRNA and immunoreactivity in the developing rat lung. With the use of RNA blot hybridization, abundant pulmonary ceNOS mRNA was detected during the late fetal and postnatal period. The highest levels were detected within 24 h after birth, and elevated mRNA levels persisted for 16 days. In contrast, much lower levels of ceNOS mRNA were found in adult rat lung. With the use of immunoblot techniques, ceNOS protein levels were found to be correlated with mRNA levels. To identify the pulmonary cell types expressing the ceNOS gene, in situ hybridization with a digoxigenin-labeled cRNA probe was performed on sections from lungs of 1-day-old and adult rats. In lungs from 1-day-old rats, ceNOS mRNA was detected in alveolar and serosal epithelial cells as well as in endothelial cells lining small and medium-sized blood vessels. In contrast, in adult lungs, ceNOS gene transcripts were detected in rare endothelial cells. These observations suggest that ceNOS gene expression is regulated during lung development and that ceNOS is available to participate in the postnatal reduction of pulmonary vascular resistance. ceNOS gene expression in nonendothelial cells in the neonatal rat lung suggests that NO may also contribute to nonvascular functions in the developing lung.

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