IS MATERNAL COPPER SUPPLEMENTATION DURING ALVEOLARIZATION PROTECTING THE DEVELOPING RAT LUNG AGAINST THE ADVERSE EFFECTS OF MATERNAL NICOTINE EXPOSURE? A Morphometric Study

Maritz, Gert S.; Windvogel, Shantal Lynn

doi:10.1080/01902140303785

Cited by 21 publications

(26 citation statements)

References 37 publications

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“…Exposure of fetal monkeys and rats to nicotine via the placenta during the late saccular/early alveolar phase of lung development results in an increase in the size and volume density of the primitive alveoli. As a consequence the alveolar surface area for gas exchange decreases (Collins et al, 1985;Maritz and Windvogel, 2003b). The structural changes in the lungs of these animals actually resemble faster aging of the lungs.…”

Section: Structural Developmentmentioning

confidence: 94%

Nicotine and lung development

Maritz

2008

Birth Defects Research Pt C

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Nicotine is found in tobacco smoke. It is a habit forming substance and is prescribed by health professionals to assist smokers to quit smoking. It is rapidly absorbed from the lungs of smokers. It crosses the placenta and accumulates in the developing fetus. Nicotine induces formation of oxygen radicals and at the same time also reduces the antioxidant capacity of the lungs. Nicotine and the oxidants cause point mutations in the DNA molecule, thereby changing the program that controls lung growth and maintenance of lung structure. The data available indicate that maternal nicotine exposure induces a persistent inhibition of glycolysis and a drastically increased cAMP level. These metabolic changes are thought to contribute to the faster aging of the lungs of the offspring of mothers that are exposed to nicotine via the placenta and mother's milk. The lungs of these animals are more susceptible to damage as shown by the gradual deterioration of the lung parenchyma. The rapid metabolic and structural aging of the lungs of the animals that were exposed to nicotine via the placenta and mother's milk, and thus during phases of lung development characterized by rapid cell division, is likely due to "programming" induced by nicotine. It is, therefore, not advisable to use nicotine during gestation and lactation.

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Section: Structural Developmentmentioning

confidence: 94%

Nicotine and lung development

Maritz

2008

Birth Defects Research Pt C

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“…Alternatively, the fetal lung may be more susceptible than other organs to the growth-retarding effects of cigarette smoking. It is also reported that nicotine exposure during pregnancy and lactation results in impaired elastic tissue formation [25] , parenchymal damage [22] , slow alveolarization [26] , hyperplasia of bronchial muscle, mesenchymal changes, and a higher incidence of apoptosis [27] in neonatal lung. However, in these studies nicotine was given to the mother during both the pregnancy and during lactation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Maternal Nicotine Exposure during Lactation on Breast-Fed Rat Pups

Özokutan¹,

Özkan²,

Sarı

et al. 2005

Neonatology

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Background: Nicotine is known to be associated with adverse effects in infants and children. It is concentrated in breast milk and is absorbed by the infant. The aim of this study was to investigate the effects on breast-fed rat pups of maternal nicotine exposure during lactation. Methods: In the experimental group (n = 6), nicotine was given to lactating dams (2 mg/kg/day) after delivery and continued for 10 days during lactation. Control animals (n = 4) received saline for the same duration. The suckling rats were weighed and killed on postnatal day 10, and samples were taken from the lung, liver, kidney, spleen and small intestine for histopathological examination. Superoxide dismutase (SOD), catalase (CAT) activities and malondialdehyde (MDA) levels were measured in the liver of the dam and the offspring. Results: Histopathological changes in the liver of the nicotine-exposed group showed portal inflammatory infiltrate, ballooning degeneration of hepatocytes, and focal necrosis in the parenchyma. Thickening of alveolar walls because of interstitial inflammation was noted in the lungs. Histopathological examination of kidney, spleen and small intestine tissue did not reveal any abnormality. In the experimental group, SOD and CAT activities were significantly decreased (p <0.001) but MDA levels were significantly increased (p <0.001) compared with the control group. Conclusion: These results indicate that maternal nicotine exposure induces oxidative stress and causes detrimental histopathological changes in the lung and liver of lactating offspring.

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“…Copper is also involved in antioxidant defences both extracellularly, when bound as ceruloplasmin (Al-Timimi & Dormandy, 1977;Goldstein et al, 1979;Gutteridge et al, 1980;A.D., Taylor & Oey, 1982), and intracellularly as a coenzyme for superoxide dismutase (Fridovich, 1978;Forsberg et al, 2001). Copper is also necessary in the diet to prevent inflammation (Denko, 1979) and emphysema in animal models (O'Dell et al, 1978), as well as reducing the adverse effects of maternal nicotine exposure on lung development in rats (Maritz & Windvogel, 2003), and so may also have a protective effect against COPD. Previous epidemiological studies have provided evidence supporting a protective effect of selenium on lung function (Hu & Cassano, 2000), but data on copper are much more limited (Sparrow et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Lung function and blood levels of copper, selenium, vitamin C and vitamin E in the general population

et al. 2005

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Background: Increased dietary intake of antioxidants has been associated with higher lung function, but few studies have used biological markers of antioxidant intake. Objective: This study aimed to determine if antioxidant status, as measured by blood levels, influences lung function. Design: Using a random subsample of 479 participants, aged 18-65 y old, from a larger cross-sectional observational study, the association of forced expiratory volume in 1 s (FEV 1 ) with plasma copper, vitamin C, vitamin E and serum selenium was assessed. Results: An s.d. increase in blood copper level was associated with a difference in FEV 1 of À48 ml (95% confidence intervals: À95, À2 ml, P ¼ 0.04), vitamin C þ 49 ml ( þ 4, þ 94, P ¼ 0.03), vitamin E À15 ml (À62, þ 32, P ¼ 0.53) and selenium þ 52 ml ( þ 7, þ 96, P ¼ 0.02). The sizes of association were not appreciably altered in a mutually adjusted model. Conclusions: Higher levels of serum vitamin C and selenium appear to be associated with higher FEV 1 . The association between higher serum copper and lower FEV 1 requires further study in view of the ubiquitous exposure to this mineral. Sponsorship: National Asthma Campaign and British Lung Foundation.

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IS MATERNAL COPPER SUPPLEMENTATION DURING ALVEOLARIZATION PROTECTING THE DEVELOPING RAT LUNG AGAINST THE ADVERSE EFFECTS OF MATERNAL NICOTINE EXPOSURE? A Morphometric Study

Cited by 21 publications

References 37 publications

Nicotine and lung development

Nicotine and lung development

Effects of Maternal Nicotine Exposure during Lactation on Breast-Fed Rat Pups

Lung function and blood levels of copper, selenium, vitamin C and vitamin E in the general population

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