Asbestos Malignancies Pulmonary Toxicity And The Mesothelioma Menace

Asbestos Malignancies Pulmonary Toxicity And The Mesothelioma Menace

Mesothelioma is a deadly disease that has claimed the lives of thousands of people. It is caused by the inhalation of asbestos dust. Although no cure has been found, continue diligent researchers to study the disease and its relationship to asbestos. An interesting study is called, "Asbestos causes apoptosis in alveolar epithelial cells: The role of iron-induced free radicals" - Journal of Laboratory and Clinical Medicine, Volume 137, Issue 5, Pages 330-339. Here is an excerpt:. "Asbestos causes asbestosis and malignancies by mechanisms that are not fully understood Alveolar epithelial cells (AEC) injury by iron-induced reactive oxygen species (ROS) is an important mechanism in order to determine whether asbestos causes in AEC apoptosis, we WI. -26 (human type I-like cells), A549 (human type II-like cells) and rat alveolar type II cells exposed to asbestos amosite and assessed apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine-5'-triphosphate-biotin nick end labeling (TUNEL) staining, nuclear morphology, annexin V staining, DNA nucleosome formation and caspase-3 activation. 

Unlike the Central and TiO2, amosite asbestos and H2O2, respectively causes AEC apoptosis control. A role for iron-catalyzed ROS was supported by the finding that asbestos-induced apoptosis AEC and caspase 3 activation were both attenuated by either an iron chelator (phytic acid and deferoxamine) or an OH scavenger (dimethyl-thiourea, salicylate, and suggested sodium benzoate), but not by iron loaded phytic acid. order to determine whether asbestos apoptosis effected in vivo, the rats received a single intra-tracheal instillation of amosite (5 mg) or saline solution, and apoptosis in epithelial cells in the bronchoalveolar channel regions assessed by TUNEL staining. One week after the exposure, amosite asbestos caused a 3-fold increase in the proportion of apoptotic cells in the bronchoalveolar duct regions (control, 2.1% ± 0.35%; asbestos, 7.61% ± 0.15%, N = 3) were compared, however. 4 weeks, the number of apoptotic cells was similar to control. We conclude that asbestos-induced pulmonary toxicity may be partly due to apoptosis in the lungs, the iron-catalyzed through epithelial ROS and caspase 3 activation is mediated caused. 

"Another interesting study is called, "Comparative proliferative and histopathologic changes in rat lungs after inhalation of chrysotile or crocidolite" by Kelly A. BéruBéa, Timothy R. Quinlana, Gerald Moultona, David Hemenwayb, Patrick O'Shaughnessyb, Pamela Vacekc and Brooke T. Mossmana - Toxicology and Applied Pharmacology - Volume 137, Issue 1, March 1996, pages 67-74. Here is an excerpt: "Patterns of cell proliferation in the lung and pleura and development of histopathological lesions in lungs were examined by Fischer 344 rats after inhalation of chrysotile or crocidolite at intermediate concentrations in the air of about 8 mg/m3air for 5 to 20 days and after followed 20 days after exposure to an additional 20 days of the room air (20 + 20 days). order to evaluate the cell proliferation Rats were injected with 5-bromo-2'-deoxyuridine (BrdU) at different time points after start of the asbestos. image analysis was used to quantify the effects of chrysotile and crocidolite on BrdU indices in the following lung compartments: (1) interstitial, (2) alveolar duct region (3), bronchial epithelium, and (4) visceral mesothelium With the exception of the mesothelium that. 

significant increases in BrdU incorporation asbestos-induced increases in BrdU incorporation into other compartments were issued in rats at 20 crocidolite + 20 days transiently transfected with labeling field comparable to sham controls at later time points. Histopathology of rat lungs revealed fibrotic lesions to a greater extent and severity at 20 days rats crocidolite, but fibrosis occurred in both asbestos-exposed groups after 20 days of clean air (20 + 20). quantification of the fiber stress in rat lung after inhalation of comparable concentrations of both fiber type demonstrated that the inhalation of crocidolite to a higher fiber retention led which in comparison to asbestos chrysotile. Our results indicate that chrysotile and crocidolite different patterns of cell proliferation induced in the lung and pleural cells. The protracted increases in BrdU labeling of mesothelial cells by crocidolite may reflect increased retention of fibers and / or inherent differences between different types of asbestos