Influence Of Maternal Nicotine Exposure Research Articles

Influence of maternal nicotine exposure on neonatal rat oxidant–antioxidant system and effect of ascorbic acid supplementation

There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.

Influence of maternal nicotine exposure during gestation and lactation on lactate dehydrogenase isoenzyme profile and transcript levels in developing neonatal rat lung

In this study we investigated the effect of (a) aging on rat lung lactate dehydrogenase (LDH) mRNA expression and isoenzyme profile and, (b) the effect of maternal nicotine exposure during gestation and lactation on LDH isoenzyme profile and mRNA expression in the lungs of the offspring. Pregnant rats were injected subcutaneously (1 mg nicotine/kg body weight/day) from day 1 after mating. Lung tissue to determine LDH isoenzyme profile and mRNA expression was obtained from the offspring. LDH mRNA expression and isoenzyme profile was determined on postnatal days 1, 7, 14, 21 and 49. Generally the %Densities of all the isoenzymes decreased between postnatal days 1 and 49. Between postnatal days 7 and 14, a period associated with rapid alveolar formation, all isoenzymes except LDH-1, decreased ( P < 0.01). During this period all the isoforms in nicotine-exposed lung increased ( P < 0.05). In both control and nicotine-exposed lung LDH-1 is the dominant isoenzyme. The LDH-M and LDH-H isoenzyme levels are higher ( P < 0.001) in the lungs of the nicotine exposed rats. Maternal nicotine exposure during gestation and lactation changed the metabolic status of the nicotine-exposed lungs to become more glycolytic compared to that of the control lung. These changes in LDH isoenzyme profiles and mRNA expression are irreversible.

Influence of maternal nicotine exposure on neonatal rat bone: protective effect of pentoxifylline.

Limited research in young adults and immature animals suggests a detrimental effect of tobacco on bone during growth. The aim of this study was to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on neonatal rat bone development, and to determine a protective effect of pentoxifylline (PTX). Gravid rats were assigned into four groups, one control (group I) and three experimental (groups II, III, and IV). In group II, pregnant rats received 3 mg/kg/day nicotine alone, subcutaneously, until 21 days postnatal. In group III, pregnant rats received nicotine (3 mg/kg/day) and PTX (60 mg/kg/day). In group IV, pregnant rats received PTX alone (60 mg/kg/day). Whole body mineral density (BMD), content (BMC), area (BA), and histopathologic and morphologic findings of the femur were determined at 21 days of age. The study revealed that nicotine exposure (group II) decreased birth weight, pregnancy weight gain, and length of femur compared with other groups (P < 0.01). Birth weight was higher in groups III (PTX + nicotine) and IV (PTX) than in group II (nicotine). Body weight at 21 days of age was higher (P = 0.009) in the PTX alone group (group IV) compared with the other groups. BMD was higher (P < 0.001) in the PTX-treated groups (group III and IV) compared with other groups. In addition, there were more apoptotic chondrocytes in the hypertrophic zone of rats exposed to nicotine alone (group II) compared with the other groups (P < 0.001). In conclusion, maternal nicotine exposure resulted in decreased birth weight, pregnancy weight gain, and bone lengthening, and increased apoptosis. Pentoxifylline supplementation was found to prevent the adverse effects of maternal nicotine exposure on BMD and birth weight.

Perinatal expression of HSP70 and VEGF in neonatal rat lung vessels exposed to nicotine during gestation

We assessed the influence of maternal nicotine exposure during gestation on perinatal expression of HSP70 and VEGF in rat lung parenchyma and lung vessels. Adult white Sprague-Dawley virgin rats were mated with adult male rats over 2 days, with two females for every male. After confirming pregnancy, 30 gravid rats (dams) were then randomly assigned to two equal groups (one experimental and one control; n=15 in each). Experimental dams were treated with subcutaneus (s.c.) (-)-nicotine tartrate, 3 mg/kg body weight/day, during pregnancy from gestational days 9 through 21. After sacrifice, lungs were removed en bloc and formalin-fixed, and paraffinembedded tissue sections were evaluated by immunohistochemistry using a three-step streptavidin-biotin-peroxidase method with monoclonal antibodies directed against HSP70 or VEGF. HSP70 and VEGF expression was increased in the vascular smooth muscle cells of the experimental group (t1) compared to the control group (t(2))t(1)=7.593, t(2)=4.666, p<0.05). The number of bronchioles that stained positively with HSP70 was higher in the nicotineexposed group than in the control group (t(1)=9.274, t(2)=6.956, p<0.05). In conclusion, gestational nicotine exposure increased the expression of VEGF and HSP70 in rat lung parenchyma, especially in the airway epithelium and vascular smooth muscle cells. In vascular smooth muscle cells, these molecules may contribute to nicotine-related hypoxic pulmonary hypertension.

Effect of nicotine exposure during gestation on neonatal rat crystalline lenses

To assess histologically the influence of maternal nicotine exposure during gestation in vivo on crystalline lenses in neonatal rats using different dosages of the test compound simulating the range of low, moderate, and heavy smokers in humans. Experimentally naive, adult female Wistar-albino rats (200-250 g) were mated with adult male rats over 2 days for copulation in the proportion of two females for every male animal. After confirming pregnancy with vaginal smear method, 40 gravid rats (dams) were then randomly assigned into four equal groups (three experimental and one control; n=10 in each). Groups 1, 2, and 3 experimental dams were treated with intraperitoneal (i.p.) (-)-nicotine tartrate at doses of 0.5, 1, and 2 mg/kg body weight/day, respectively, during pregnancy from gestational days 9 through 21. Group 4 control dams were given i.p. saline solution daily for the same period. After normal delivery, the eyes were removed at postnatal day 1 or day 30 for macroscopic and histopathologic investigation of the lenses. Control and group 1 litters had normal anterior lens capsules with a single layer of anterior cuboidal epithelial cells, regularly orientated cortical and nuclear lens fibres, and a clear posterior lens capsule with no lining epithelial cells behind the equator. On the other hand, some lenses in groups 2 and 3 litters had mature or immature cataract macroscopically at postnatal 30th day. Histopathologic findings suggesting cataractogenesis included cortical lens fibre cell swelling and liquefaction, prominent epithelial cells lining the posterior lens capsule behind the equator, and the retention of lens nuclei into the deeper and central area. Moreover, some lenses were immature developmentally, indicating arrested lenticular embryogenesis at vesicle stage. Nicotine exposure during pregnancy has teratogenic and cataractogenic effects on developing crystalline lenses in neonatal rats both macroscopically and histopathologically. If appropriate dose of nicotine can be identified, nicotine-induced cataract formation may possibly be used as a new experimental cataract model in animal studies. Therefore, future studies are needed in this respect. Eye (2004) 18, 67-73. doi:10.1038/sj.eye.6700511

The influence of maternal nicotine exposure on key enzymes of glucose metabolism in lung tissue of the offspring

Abstract In this study the influence of maternal nicotine exposure during gestation and lactation on selected enzymes of the glycolytic pathway of lung tissue of 1, 7, 14 and 21 day-old neonatal rat pups were investigated. The results clearly show that maternal nicotine exposure had no influence on the activity of hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase or glucose-6-phosphate dehydrogenase of lung tissue of the offspring of the various age groups. Maternal nicotine exposure also had no influence on the cytoplasmic NADH/NAD ratio of the lung tissue of the offspring. The activity of glyceraldehyde-3-phosphate dehydrogenase (GAPD) of lung tissue of control rat pups increased from day 7 after birth and reached optimal activity on day 14 after birth. On days 1 and 7 after birth, the GAPD activity of lung tissue of nicotine exposed rat pups was the same as for control lung. However, in contrast to control lung, no increase in GAPD activity occured in lung tissue of nicotine exposed rat pups between days 7 and 14 after birth. It is suggested that this interference with GAPD development as the lung matures may interfere with glycolysis and the development and maintenance of the alveolar epithelium of the developing rat lung.

Maternal nicotine exposure induces microscopic emphysema in neonatal rat lung

Abstract The influence of maternal nicotine exposure (1 mg/kg body mass per day, SC) on neonatal lung morphology and morphometry was studied. The results show that maternal nicotine exposure during gestation and lactation induced alveolar damage which was reflected in alveolar epithelial membrane blebs, fenestrations, a reduced radial alveolar count, an increased destructive index and percentage abnormal alveolar attachments. These findings indicate that maternal nicotine exposure induce microscopic emphysema in the lungs of the offspring.

The influence of maternal nicotine exposure on the status of the connective tissue framework of developing rat lung

The aim of the present study was to investigate the effect of maternal nicotine exposure on the status of the connective tissue framework of neonatal rat lung. From the data it is clear that maternal nicotine exposure had no influence on the collagen content of the lung tissue of the offspring. The elastic tissue content on day 7 after birth was higher ( P < 0.05) than in control lung of rat pups of the same age. The rate of elastic tissue formation was, at 431.4 μg/g lung tissue per day, 53.6% higher ( P < 0.05) than in nicotine-exposed lung. On days 14 and 21 after birth, the elastic tissue content of the lungs of the control and nicotine-exposed lungs were the same. Maternal nicotine exposure however interfered with the 3D structure of the connective tissue framework. This may reduce the stability of this framework and render the lung more susceptible to stress injury.

Maternal nicotine exposure: reponse of type II pneumocytes of neonatal rat pups.

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.

Biomedical response of neonatal rat lung to maternal nicotine exposure

The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical response of neonatal lung was investigated. Maternal nicotine exposure during pregnancy suppressed glycolysis irreversibly and thus energy supply to especially type I epithelial cells. The lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and glucose 6-phosphate dehydrogenase (G6PDH) activity in bronchoalveolar lavage (BAL) increased, thereby indicating damage to type I and II cells. The lower total lung G6PDH activity of the neonatal lungs exposed to nicotine might reduce the capacity of the lung to protect itself against foreign substances to which it is exposed, thereby rendering it more susceptible to damage.

The influence of maternal nicotine exposure on neonatal lung metabolism. Protective effect of ascorbic acid.

The aim of the present study was to establish whether ascorbic acid supplementation (1 mg/kg/body mass/day) during pregnancy and lactation will prevent the effect of maternal nicotine exposure (1 mg/kg body weight/day) on neonatal lung carbohydrate, DNA and protein metabolism. The data show that the adult lung ascorbic acid content was reduced by 76% after exposure to nicotine. In contrast, maternal nicotine exposure during pregnancy and lactation has no effect on neonatal lung ascorbic acid content. However, ascorbic acid supplementation during pregnancy and lactation prevented the adverse effects of maternal nicotine exposure on neonatal lung carbohydrate, DNA and protein metabolism.

The influence of maternal nicotine exposure on neonatal lung carbohydrate metabolism

The influence of maternal nicotine exposure (1 mg/kg body mass/day) during pregnancy and lactation on energy metabolism of lung tissue of neonatal rats were investigated. The glucose turnover of the lung tissue of the neonatal rats exposed to nicotine via the placenta and mother's milk was 86,4% higher than that of the controls. Glycolysis was however suppressed by 22,7% (P<0,01). The adenine nucleotide pool (ATP + ADP + AMP) was 32,8% higher for the lungs of the 3 week old neonates exposed to nicotine than that of the control rat lung. After 4 weeks of nicotine withdrawal glycolysis of those animals exposed to nicotine were still inhibited to the same extent than during exposure. The adenine nucleotide pool was 69,95% higher than that of the controls. It is proposed that the inhibition of glycolysis was due to the high ATP/ADP ratio of the lungs of the nicotine exposed rats.