Development of Asbestos Related Pulmonary Disorders and Mesothelioma
One interesting study is called, "Early Inflammatory Response to Asbestos Exposure
in Rat and Hamster Lungs: Role of Inducible Nitric Oxide Synthase" by Martina Drgera, , Anne-Marie Allmelinga, Rainer Kiefmannb, Silvia Mnzinga, Konrad Messmera and Fritz Krombacha - Toxicology and Applied Pharmacology - Volume 181, Issue 2, 1 June 2002, Pages 93-105. Here is an excerpt: "Abstract - Recent studies have suggested that inducible nitric oxide synthase (iNOS) plays a role in the development of asbestos-related pulmonary disorders. The pulmonary reactions of rats and hamsters upon exposure to asbestos fibers are well known to be disparate. In addition, in vitro experiments have indicated that mononuclear phagocytes from hamsters, in contrast to those from rats, lack the iNOS pathway. Therefore, the purpose of this study was to investigate whether rats and hamsters differ in lung iNOS expression in vivo upon exposure to asbestos fibers and whether differences in iNOS induction are associated with differences in the acute pulmonary inflammatory reaction. Body weight, alveolararterial oxygen difference, differential cell count in bronchoalveolar lavage fluid, total protein leakage, lung myeloperoxidase activity and lipidperoxidation, wet/dry ratio, iNOS mRNA and protein expression, and nitrotyrosine staining of lung tissue were determined 1 and 7 days after intratracheal instillation of asbestos fibers in CD rats and Syrian golden hamsters. Exposure of rats to asbestos fibers resulted in enhanced pulmonary iNOS expression and nitrotyrosine staining together with an acute inflammation that was characterized by an influx of neutrophils, enhanced myeloperoxidase activity and lipid peroxidation, damage of the alveolarcapillary membrane, edema formation, and impairment of gas exchange. In comparison, instillation of asbestos fibers in hamsters resulted in a significantly milder inflammatory reaction of the lung with no induction of iNOS in pulmonary cells. The data obtained provide important information to understand the underlying mechanisms of species differences in the pulmonary response upon exposure to asbestos fibers."
Another interesting study is called, "Energy restriction that inhibits cellular proliferation by torpor can decrease susceptibility to spontaneous and asbestos-induced lung tumors in A/J mice." By Koizumi A, Tsukada M, Hirano S, Kamiyama S, Masuda H, Suzuki KT. -
Lab Invest. 1993 Jun;68(6):728-39. Here is an excerpt: "Abstract - BACKGROUND: Energy restriction (ER) inhibits various tumors in mice. A/J mice have a very high incidence of lung tumors, that are correlated with elevated levels of pulmonary cell proliferation in this strain. Using A/J mice, we studied the effects of ER on spontaneous and asbestos-induced lung tumors and on labeling indices in the lung as a proximal marker of susceptibility to lung tumors to obtain better understanding of the mechanism of ER in reducing tumorigenesis. EXPERIMENTAL DESIGN: Experiment 1: A/J female mice were instilled intratracheally with asbestos or titanium dioxide or simple saline at 20 weeks of age. At 21 weeks of age, mice of the ER diet group were switched from the control diet (350 kJ/week) to the ER diet (175 kJ/wk) until sacrifice at 105 weeks of age, whereas mice of the control diet group were continued on the control diet. Experiment 2: A/J female mice were begun on ER or control diets at 6 weeks of age. The control and ER mice were kept at 20 to 22 degrees C, whereas mice of another ER group (ER+I) were kept at 30 degrees C until 24 weeks of age. Body temperatures of these mice were monitored by telemetery.
RESULTS: The present ER was shown to suppress the development of both asbestos-induced and spontaneous lung tumors. ER mice were confirmed to become torporfic, whereas control and ER+I mice did not. Labeling indices were reduced by ER in the lung as well as in other organs. The reduction of labeling indices was, however, almost recovered by increasing the housing temperature to 30 degrees C. CONCLUSIONS: ER which reduces cellular proliferation in various organs by torpor was shown to inhibit lung tumors. Inhibition of lung tumors by ER is likely to involve a decrease in cell proliferation."
Another interesting study is called, "Autocrine Growth Stimulation by Transforming Growth Factor in Asbestos-transformed Rat Mesothelial Cells" by Cheryl Walker, Jeffrey Everitt, Patrice C. Ferriola, Wendy Stewart, James Mangum, and Edilberto Bermudez - Cancer Res February 1, 1995 55; 530. Here is an excerpt: "Abstract - Although the association between asbestos exposure and mesothelioma development has been established for decades, very little is known regarding the molecular mechanism(s) by which asbestos fibers induce this disease. In this series of experiments, the potential for transforming growth factor (TGF-) to act as an autocrine growth factor in transformed mesothelial cells was examined in rats, a model system frequently used to assess the tumorigenic potential of fibrous particulates. Both asbestos-transformed cells and spontaneously transformed cells expressed functional EGF receptors, although only the asbestos-transformed cells expressed TGF-. Expression of TGF- transcripts was correlated with secretion of picogram amounts of growth factor into conditioned medium by the asbestos-transformed cells. In addition, whereas TGF- inhibited the growth of spontaneously transformed mesothelial cells, it stimulated the growth of asbestos-transformed cells. Neutralizing antibody that recognized TGF- secreted by the asbestos-transformed cells was able to inhibit the growth of these cells. Taken together, these data indicate that TGF- acts as an autocrine growth factor for asbestos-transformed rat mesothelial cells. Therefore, in asbestos-transformed mesothelial cells, altered production and responsiveness to TGF- distinguish these cells from spontaneously transformed mesothelial cells. These data suggest that differences in mesothelioma etiology may be reflected in differences in the molecular alterations present in these tumors."
Development of Asbestos Related Pulmonary Disorders and Mesothelioma
By: Montwrobleski77
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