The influence of maternal nicotine exposure on the interalveolar septal status of neonatal rat lung.

Maritz, Gert S.; Thomas, Richard

doi:10.1006/cbir.1994.1104

Cited by 25 publications

(17 citation statements)

References 7 publications

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“…Collins et al (8) exposed pregnant rats to cigarette smoke and similarly found enlarged and fewer saccules in fetal rats after cigarette smoke exposure. Maritz et al (9,42) treated rats with a combination of pre-and postnatal nicotine and similarly found decreased radial alveolar count and increased mean linear intercept in neonatal rats. The finding that nicotine alters alveolar development in both monkeys and rodents makes it highly likely that prenatal exposure to nicotine will similarly affect human lung development.…”

Section: Discussionmentioning

confidence: 96%

Prenatal nicotine increases pulmonary α7 nicotinic receptor expression and alters fetal lung development in monkeys

Sekhon¹,

Jia²,

Raab³

et al. 1999

J. Clin. Invest.

293

244

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It is well known that smoking during pregnancy is the largest preventable cause of low birth weight, premature delivery, neonatal morbidity, and mortality (1, 2). Perhaps less well appreciated is the recent, strong evidence that smoking during pregnancy directly and adversely effects lung development, as manifested by altered pulmonary function and increased respiratory illness in children born of smoking mothers (3-6). Stoddard and Gray (7) recently estimated that annual costs of increased respiratory illness associated with maternal smoking is in excess of 660 million dollars per year. How smoking produces these effects is not fully understood. While the cause of pulmonary damage caused by maternal smoking is likely to be multifactorial, evidence presented in this paper indicates that much of the effect of maternal smoking on the lung may be mediated by the interaction of nicotine with nicotinic receptors expressed in the developing lung.Multiple studies have shown increased lower respiratory illness in infants born of mothers who smoke (3, 4). Taylor and Wadsworth (3) studied 12,743 children and found significantly increased bronchitis and hospital admissions for lower respiratory illness in children from smoking mothers. Significantly increased hospital admissions were not seen for children whose mothers smoked only after pregnancy, arguing for a prenatal effect. Tager et al. (4) similarly found increased lower respiratory illness with prenatal smoke exposure, but not with postnatal exposure. Correlating the increased respiratory illness with altered pulmonary function, Hanrahan et al. (5) examined pulmonary function of infants shortly after birth (∼4.2 weeks) as a function of smoking during pregnancy (determined both by questionnaire and by urinary cotinine) and found decreased respiratory flow rates. In a follow-up study, Tager et al. (4) showed that the decreased ventilation at functional residual capacity (VFRC) seen with prenatal smoke exposure correlated directly with increased lower respiratory illnesses. Cunningham et al. (6) performed pulmonary function tests on 8,800 nonsmoking school children 8-12 years old and similarly found reduced forced expiratory flow in children whose mothers smoked during pregnancy. Again the correlation was with prenatal, not postnatal, maternal smoking. This confirmed the earlier studies and suggested the deficit continued at least to adolescence.Animal studies on the effects of smoking or nicotine on lung development have been quite limited, and there have been no studies of potential molecular mechanisms. It is well established that maternal smoking during pregnancy is a leading preventable cause of low birth weight and prematurity. Less appreciated is that maternal smoking during pregnancy is also associated with alterations in pulmonary function at birth and greater incidence of respiratory illnesses after birth. To determine if this is the direct result of nicotine interacting with nicotinic cholinergic receptors (nAChRs) during lung development, rhesus monkeys w...

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Section: Discussionmentioning

confidence: 96%

Prenatal nicotine increases pulmonary α7 nicotinic receptor expression and alters fetal lung development in monkeys

Sekhon¹,

Jia²,

Raab³

et al. 1999

J. Clin. Invest.

293

244

View full text Add to dashboard Cite

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“…Previous studies have shown that nicotine treatment not only causes swelling and structural remodeling of mitochondria in cells of various tissues, including the brain (Jin and Roomans 1997; Maritz and Thomas 1994; Onal et al 2004; Zimmerman and McGeachie 1987), but also regulates processes such as protein turnover (Katyare and Shallom 1988), enzyme activity (Barbieri et al 1989; Galvin et al 1988), and generation of ROS (Bhagwat et al 1998; Soto-Otero et al 2002). Here, we further demonstrate that the genes of each complex in the electron transfer system are modulated by chronic nicotine treatment.…”

Section: Discussionmentioning

confidence: 99%

Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions

et al. 2009

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The mitochondrion is the organelle responsible for generation of most usable energy in a cell. It also plays an important role in a series of physiological processes such as apoptosis and proliferation. Although previous studies have demonstrated that nicotine modulates the morphology and function of mitochondria, the mechanism(s) underlying these effects is largely unknown. In this study, using a microarray consisting of 4,793 clones derived from a mouse dopamine cDNA library, we profiled the gene expression patterns for six brain regions (amygdala, hippocampus, nucleus accumbens, prefrontal cortex, striatum, and ventral tegmental area) of female Sprague-Dawley rats subjected to nicotine treatment for 7 days through osmotic minipump infusion. We identified a number of genes and pathways, including components of the electron transport system of mitochondria, such as cytochrome c oxidase subunit I (Mt-co1), Mt-co2, Mt-co3, cytochrome b (Mt-cyb), mitochondrial NADH dehydrogenase 4 (Mt-nd4), and Mt-nd6, that were significantly modulated by nicotine in multiple brain regions. Bioinformatics analysis provided evidence that Gene Ontology categories related to the electron transport system were overrepresented in each brain region. Finally, the results from the microarray analysis were verified by quantitative RT-PCR for four representative genes. Together, our findings imply that mitochondria are involved in neuronal adaptation to chronic nicotine exposure.

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Section: Structural Developmentmentioning

confidence: 95%

“…As a consequence of the proliferation of the alveolar type II cells, the type I/type II cell ratio decreased in the lungs of these animals (Maritz and Thomas, 1994). Nicotine also stimulates surfactant synthesis in type II cells (Maritz and Thomas, 1994;Rehan et al, 2007). Pulmonary fibroblasts are thought to be positive modulators of this process through the synthesis of keratinocyte and hepatocyte growth factors, both known to be potent mitogens for type II cells (Panos et al, 1993).…”

Section: Structural Developmentmentioning

confidence: 95%

“…Alveolar type II cells have been found to be increased in the lungs of nicotine exposed animals, which is thought to be a response to type I cell damage and death (Maritz and Thomas, 1994). As a consequence of the proliferation of the alveolar type II cells, the type I/type II cell ratio decreased in the lungs of these animals (Maritz and Thomas, 1994).…”

Section: Structural Developmentmentioning

confidence: 99%

See 1 more Smart Citation

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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The influence of maternal nicotine exposure on the interalveolar septal status of neonatal rat lung.

Cited by 25 publications

References 7 publications

Prenatal nicotine increases pulmonary α7 nicotinic receptor expression and alters fetal lung development in monkeys

Prenatal nicotine increases pulmonary α7 nicotinic receptor expression and alters fetal lung development in monkeys

Significant modulation of mitochondrial electron transport system by nicotine in various rat brain regions

Nicotine and lung development

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