<p>Tobacco smoking during pregnancy and lactation is a common habit and accounts for a significant percentage of fetal morbidity and mortality worldwide. The offspring is as a result exposed to nicotine through the blood and the milk of the mother. Nicotine is thus expected to interact with the developing fetus and the offspring of mothers who smoke or use NRT for smoking cessation, resulting in the interference with normal fetal and neonatal lung development. Maternal cigarette smoke or nicotine exposure produces adverse effects in the lungs of offspring, these include / intrauterine growth retardation, low birth weight, premature birth, reduced pulmonary function at birth, and a high occurrence of respiratory illnesses after birth. This study aimed at investigating&nbsp / the effects of maternal nicotine exposure during gestation and lactation on lung development in the offspring / to establish whether tomato juice can have protective effects on the fetal lung&nbsp / development and function in the offspring / and to determine if nicotine cases premature aging of the lungs of the offspring. It was therefore shown that maternal exposure to nicotine during&nbsp / gestation and lactation ad no significant effect on the growth parameters of the offspring. Maternal nicotine exposure during gestation and lactation had no effect on the growth parameters of&nbsp / the offspring, but resulted in compromised lung structure and function. The morphometric results demonstrated decrease in alveolar number, increase in alveolar size, and decrease in lung&nbsp / parenchyma of the nicotine exposed animals showing a gradual deterioration of the lung parenchyma. Structural alterations include emphysematous lesions, where the latter was&nbsp / accompanied by an increase in alveolar size (Lm), and a decrease in the tissue volume of the lung parenchyma. Thickening of alveolar walls was also evident and serves as an indication of&nbsp / remodeling of the extracellular matrix, also a characteristic of emphysema. A consequence of the gradual deterioration of the lung parenchyma is a decrease in the alveolar surface area available for gas exchange. The present study showed that the emphysematous lesions were conceivably a result of a reduced rate of cell proliferation accompanied by the increase in&nbsp / senescent cells numbers in the alveolar walls of the exposed offspring. The data of this study suggests that maternal nicotine exposure during gestation and lactation induces premature&nbsp / aging of the lungs of the offspring rendering the lungs of the offspring more susceptible to disease later in life. Since these structural changes occurred later in the life of the offspring and long&nbsp / after nicotine withdrawal, it is suggested that it is programmed during gestation and lactation. Smoking and NRT result in an increased load of oxidants in the mother and fetus. It also reduces&nbsp / the level of anti-oxidants and thereby compromising the ability of the mother to protect the fetus. It is hypothesized that this oxidant-antioxidant imbalance will program the lungs to age&nbsp / prematurely. The supplementation of the mother&rsquo / s diet with tomato juice, rich in lycopene, other anti-oxidants such as vitamin C, as well as phytonutrients protected the lungs of the offspring&nbsp / against the adverse effects of maternal nicotine exposure. This supports the hypothesis mentioned above. The study further showed that the effects of grand-maternal nicotine exposure during gestation and lactation on the lungs of the F1 offspring is also transferred to the F2 offspring. This is most likely via the paternal and maternal germ line. Since tomato juice supplementation of the mother&rsquo / s diet with tomato juice prevented&nbsp / the adverse effects of maternal nicotine exposure on the lungs of the offspring, it is conceivable that it will prevent transfer of these changes to the F2 generation.&nbsp / </p>

Magister Scientiae (Medical Bioscience) - MSc(MBS) / Nicotine exposure to the fetus through tobacco smoking or nicotine replacement therapy during the whole period of gestation and lactation causes diverse effects on fetal and neonatal lung development, integrity and maturation which compromise the gas exchange function of the lungs and renders this vital organ susceptible to gradual damage and different diseases in latter life. Maternal nicotine exposure during gestation and lactation results in gradual destruction of the lung parenchyma, and this leads to the combination of many small air sacs in one bigger alveoli which is a sign of emphysema. Many researchers speculated that the way in which, nicotine causes emphysema and other damage, is by inducing the formation of many reactive oxygen species (ROS), and creating an imbalance between the oxidants and the antioxidants of the body, which is termed oxidative stress. The aim of this study was to assess the effects of nicotine exposure on the lung of the fetal and neonate rat during gestation and lactation as gas exchanger, and also to see whether the supplementation of tomato juice containing lycopene, a powerful carotenoid antioxidant could protect the lungs against these effects of maternal nicotine exposure. In this study pregnant rats have been divided into 4 groups: a group which received nicotine (1mg/kg body weight/day) subcutaneously, a group that received the tomato juice only (6mg/kg body weight/day per os), a third group that received the combination of tomato juice ( 6mg /kg body weight/ day per os) and nicotine (1mg/kg body weight /day subcutaneously ) . The control group that received saline (1mg/kg body weight /day) subcutaneously and water. The injections were done during pregnancy and lactation until weaning at postnatal day 21. The results showed that maternal nicotine exposure during gestation and lactation leads to a gradual damage of the lung parenchyma and slower formation of the alveoli during the equilibrated phase of the lung growth leading to a decrease in the internal surface area required for gas exchange. Supplementation with tomato juice during gestation and lactation prevents all the adverse effects of maternal nicotine exposure on the lungs of the offspring. Since nicotine induce an increase in the oxidant levels of the mother and the fetus, my results imply that lycopene protected the lungs of the offsprings against the oxidants and thus against changes in the program that controls lung development as the animals age. This is supported by the observation that at postnatal day 84 the antioxidant. / South Africa

Philosophiae Doctor - PhD / exposed to nicotine through the blood and the milk of the mother. Nicotine is thus expected to interact with the developing fetus and the offspring of mothers who smoke or use NRT for smoking cessation, resulting in the interference with normal fetal and neonatal lung development. Maternal cigarette smoke or nicotine exposure produces adverse effects in the lungs of offspring, these include; intrauterine growth retardation, low birth weight, premature birth, reduced pulmonary function at birth, and a high occurrence of respiratory illnesses after birth. This study aimed at investigating the effects of maternal nicotine exposure during gestation and lactation on lung development in the offspring; to establish whether tomato juice can have protective effects on the fetal lung development and function in the offspring; and to determine if nicotine cases premature aging of the lungs of the offspring. It was therefore shown that maternal exposure to nicotine during gestation and lactation ad no significant effect on the growth parameters of the offspring. Maternal nicotine exposure during gestation and lactation had no effect on the growth parameters of the offspring, but resulted in compromised lung structure and function. The morphometric results demonstrated decrease in alveolar number, increase in alveolar size, and decrease in lung parenchyma of the nicotine exposed animals showing a gradual deterioration of the lung parenchyma. Structural alterations include emphysematous lesions, where the latter was accompanied by an increase in alveolar size (Lm), and a decrease in the tissue volume of the lung parenchyma. Thickening of alveolar walls was also evident and serves as an indication of remodeling of the extracellular matrix, also a characteristic of emphysema. A consequence of the gradual deterioration of the lung parenchyma is a decrease in the alveolar surface area available for gas exchange. The present study showed that the emphysematous lesions were conceivably a result of a reduced rate of cell proliferation accompanied by the increase in senescent cells numbers in the alveolar walls of the exposed offspring. The data of this study suggests that maternal nicotine exposure during gestation and lactation induces premature aging of the lungs of the offspring rendering the lungs of the offspring more susceptible to disease later in life. Since these structural changes occurred later in the life of the offspring and long after nicotine withdrawal, it is suggested that it is programmed during gestation and lactation. Smoking and NRT result in an increased load of oxidants in the mother and fetus. It also reduces the level of anti-oxidants and thereby compromising the ability of the mother to protect the fetus. It is hypothesized that this oxidant-antioxidant imbalance will program the lungs to age prematurely. The supplementation of the mother’s diet with tomato juice, rich in lycopene, other anti-oxidants such as vitamin C, as well as phytonutrients protected the lungs of the offspring against the adverse effects of maternal nicotine exposure. This supports the hypothesis mentioned above. The study further showed that the effects of grand-maternal nicotine exposure during gestation and lactation on the lungs of the F1 offspring is also transferred to the F2 offspring. This is most likely via the paternal and maternal germ line. Since tomato juice supplementation of the mother’s diet with tomato juice prevented the adverse effects of maternal nicotine exposure on the lungs of the offspring, it is conceivable that it will prevent transfer of these changes to the F2 generation. / South Africa

>Magister Scientiae - MSc / Tobacco consumption and exposure to tobacco smoke is one of the biggest contributing factors to a growing epidemic of non-communicable diseases (NCDs), primarily cancers, diabetes, cardiovascular and chronic lung diseases which account for 63% of all deaths worldwide (WHO, 2011). An increased concern is in pregnant women who smoke. They not only expose themselves to nicotine, but also their unborn child. Cigarette smoking during pregnancy is associated with many developmental and growth complications. There are critical periods within the “program” that directs normal growth and development, during which the fetus is vulnerable to the effects of external factors. During these critical periods of development the program can be changed to increase the susceptibility of the fetal organs to disease and increased risk of adverse health consequences in adulthood. Health care professionals have tried to reduce the consumption of tobacco smoke by prescribing nicotine replacement therapy (NRT) to pregnant females as an alternative to smoking, without considering the effects of nicotine on the developing embryo and the health risk that might arise after birth. It is known that nicotine induces oxidant formation with resulting oxidative effects. This induces an overload of oxidants in the fetus and a decrease in the antioxidant capacity thereof. This may interfere with normal lung development.

Magister Scientiae (Medical Bioscience) - MSc(MBS) / Cigarette smoking is one of the foremost causes of chronic obstructive pulmonary diseases such as emphysema and chronic bronchitis, and although it is the most preventable causes of death, it accounts for approximately 6 million deaths worldwide each year. Cigarette smoking during pregnancy and lactation remains one of the primary modifiable risk factors for undesirable fetal, obstetrical, and developmental outcomes. Consequently, the offspring of the smoking mother is exposed to nicotine via the blood and the milk of the mother. As a result, nicotine interacts with the developing offspring and therefore interferes with normal fetal lung development. Maternal smoking during gestation and lactation has been associated with both short and long term health risks ranging from intrauterine growth restriction to physiological abnormalities. Maternal smoking has also been strongly linked to an increased risk for pulmonary diseases and respiratory morbidity in the offspring of the smoking mother. The main objectives of this study were to determine the effects of maternal nicotine exposure during gestation and lactation on the alveolar wall composition during lung development in the offspring; if maternal nicotine exposure during gestation and lactation induces premature cellular senescence in the lungs of the offspring; to clarify the role of pulmonary fibroblasts in premature senescence; and to establish whether tomato juice supplementation will prevent premature aging in the lungs of rats that were exposed to nicotine via the placenta and mother’s milk. From the data generated in this study it was evident that maternal nicotine exposure during gestation and lactation compromises the gas exchange function of the lungs of the F1 offspring. This was prevented by supplementing the mother’s diet with tomato juice which is then received by the offspring via the placenta and mother’s milk. This is conceivably achieved by maintaining the oxidant-anti-oxidant ratio of the mother and of the developing fetus and neonate, thereby averting premature senescence caused by nicotine exposure. Moreover, the present study also demonstrates that a decrease in fibroblast density is associated with emphysematous-like lesions in the lungs of the nicotine exposed F1 progeny. Since pulmonary fibroblasts are chief contributors to the extracellular matrix of the lungs, involved in alveolar multiplication and regeneration; premature aging or cessation of the metabolically active fibroblasts largely contributes to diminished lung structure and function.

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The quality and shelf-life of pressure processed (150, 200 and 250 MPa at 25 and 35&deg / C for 5, 10 and 15 minutes) orange, tomato and carrot juices were compared to fresh and thermally pasteurised (60&deg / C for 5, 10 and 15 minutes and 80&deg / C for 1 minute) juices. Treatments were capable of microbial inhibition of juices to non-detectable levels. The change in ascorbic acid content of HHP treated juices was not statistically significant (p&gt / 0.05). Both heat treatments at 60 and 80&deg / C, displayed a significant loss and induced a decrease in the free radical scavenging activity but was not affected by HHP treatments. Pressurization at 250 MPa at 35&deg / C for 15 minutes and thermal pasteurization at 80&deg / C for 1 minute and stored at 4 and 25&deg / C for shelf-life analysis. HHP treated juices showed a small loss of antioxidants (below 10%) at both storage temperatures whereas the loss is higher (about 30%) in the heat treated juices through shelf life (30 days). The pressurized juices, stored at 25&deg / C, contained ascorbic acid better than heat treated ones after 30 days. The total color changes were minor (&amp / #8710 / E=10) for all pressurized juices but for heat pasteurized samples, higher as a result of insufficient antioxidant activity. The pH of juices was not affected by treatment, storage temperature or time. HHP yielded a better product, regarding the studied parameters of the juices compared to the conventional pasteurization. Therefore, HHP treatment (250 MPa, 35&deg / C for 15 minutes) can be recommended for industrial production of fresh fruit and vegetables.

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