Background: Cigarette smoke is a major source of free radicals and oxidative stress. With a significant proportion of women still smoking during pregnancy, this common and avoidable exposure has the potential to influence infant oxidative status, which is implicated in the increased propensity for airway inflammation and asthma. The aim of this study was to examine the effects of maternal smoking on markers of infant oxidative stress. Methods: The level of oxidative stress (using urinary F 2 -isoprostanes as a marker of lipid peroxidation) was compared in infants of smokers (n = 33) and non-smokers (n = 54) at 3 months of age. These groups were balanced for maternal atopy and socioeconomic status. Infant urinary cotinine levels were also measured as an indicator of early postnatal cigarette smoke exposure. Results: Maternal smoking was associated with significantly higher infant cotinine levels, despite the fact that most smoking mothers (83.8%) claimed not to smoke near their baby. Maternal smoking was associated with significantly higher markers of oxidative stress (F 2 -isoprostane) at 3 months of age. There was also a positive correlation between urinary F 2 -isoprostanes and infant urinary cotinine levels. Conclusions: Although this study does not separate the prenatal and postnatal effects of smoking, these findings indicate that environmental tobacco smoke in the early postnatal period adversely affects prooxidative/antioxidative status within weeks of life in very early infancy.
The influence of maternal nicotine exposure during pregnancy and lactation on the Type II cells of lung tissue of one day old neonatal rat pups was investigated. The results clearly show that maternal nicotine exposure resulted in an increase in the type II cell count in the lungs of the offspring. In addition the lamellar body content of the type II cells of the nicotine exposed rat pups were significantly (P < 0.01) higher than that of the control animals. The type II cell mitochondria of lung tissue of nicotine exposed rat pups were swollen and no microvilli occurred on the alveolar surface. This clearly illustrates that nicotine interfered with type II cell integrity of tlte neonatal lung and may subsequently interfere with the normal development of the alveolar region of the lung.
The aim of this study was to determine the effect of maternal nicotine exposure (1 mg nicotine/kg body mass/day, subcutaneously) on the status of the alveolar septa of the 1 to 21 day old offspring. The data obtained showed swelling of type II and interstitial cell mitochondria. The type I:type II cell ratio decreased as a result of type II cell proliferation. The number of capillaries per unit length of septum was also significantly lower than that of control lung. Ruptured blood-air barriers also occur in the nicotine exposed lungs of rats of all age groups. The results show that maternal nicotine exposure interfered with the morphometric and morphologic characteristics of the septa of lung tissue of the offspring.
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