Nicotine decreased articulation of fibronectin in infant lung parenchyma


Ruhollah Ali Jobrani, Mohammed Farahani and Rudi E. Yonan

Smoking during pregnancy may impair pulmonary function in infants and children. Nicotine is one of the chemical substances with high level of toxicity. It crosses the placenta and accumulates in the developing organs of fetus. Previous investigations indicated that maternal nicotine exposure induces abnormal collagen IV expression and causes defects in bronchopulmonary development. In this study, the effect of maternal nicotine exposure on fibronectin expression in the lungs of newborn mice has been evaluated. Female Balb/C mice were mated and positivity in vaginal plug was designated as day 0 of pregnancy. Pregnant mice were divided into 2 experimental and 2 control groups. The experimental group 1 received 3 mg/kg intra peritoneal (IP) nicotine from day 7 of gestation to the last day of pregnancy. Also, the same amount of nicotine was injected into experimental group 2 during the same gestational days as well as day 14 after birth (lactation). However, control groups received the same volume of normal saline during the same periods. At the end of exposure times, all of newborns were anesthetized and their lungs removed for Immunohistochemical method and real-time polymerase chain reaction (PCR). Our finding indicated that fibronectin mRNA expression in the lung of newborn during gestation and lactation period was decreased by 0.7-and 1-fold, respectively compared with control groups. Fibronectin immunoreactivity intensity was not similar in the different parts of the lungs including alveoli, bronchiole and small vessels, having a significant decrease in immunoreactivity of the experimental groups in contrast with the control groups. These data also indicate that maternal nicotine exposure may induce abnormal fibronectin expression which may cause defects in lung function during life time. 

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