Cell Free System In The Presence Of Asbestos And Ascorbic Acid
One interesting study concerning the relationship between asbestos exposure and disease is called
, Asbestos-derived reactive oxygen species activate TGF-1 - Laboratory Investigation (2004) 84, 10131023. Here is an excerpt: Abstract - Transforming growth factor-beta1 (TGF-1) is a potent peptide that inhibits epithelial and mesenchymal cell proliferation and stimulates the synthesis of extracellular matrix components. This cytokine is produced in a biologically latent complex bound to a latent-associated peptide (LAP), and it is the disassociation of this complex that regulates TGF- activity. A number of mechanisms have been shown to activate TGF-1. We show here that reactive oxygen species (ROS), generated by the iron in chrysotile or crocidolite asbestos, mediate the biological activity of TGF-1. Recombinant human latent TGF-1 was activated in a cell free system in the presence of asbestos and ascorbic acid. Latent TGF-1 was overexpressed in both A549 and mink lung epithelial cell lines through an adenovirus vector containing the full-length construct for porcine TGF-1. This latent TGF-1 was activated in a concentration-dependant fashion by introducing asbestos into the cell cultures. This activation was reduced significantly through the use of superoxide dismutase, catalase or deferoxamine. Amino-acid constituents of the LAP were oxidized as demonstrated by the appearance of carbonyls detected by Western analysis. The oxidized LAP could no longer form a complex with TGF-1. Our data support the postulate that ROS derived from asbestos provide a mechanism for activating TGF-1 in the alveolar environment by oxidizing amino acids in LAP.
Another study is called, Mesothelioma relative to asbestos, radiation, and methylcholanthrene by Warren, S. ; Brown, C.E. ; Chute, R.N. ; Federman, M. - Arch. Pathol. Lab. Med.; (United States); Journal Volume: 105:6. Here is an excerpt: Abstract The carcinogenicity of chrysotile asbestos fibers (Canadian and Rhodesian) for the mesothelium of pleura and peritoneum of NEDH rats was explored by injection of 2 mg of asbestos fibers suspended in saline intratracheally, intrapleurally, or intraperitoneally, with or without ancillary radiation treatment (1,000 rad to the whole body of parabiont rats or 2,000 rad to the right thorax of single rats), or alternatively, by injection of asbestos plus 1 mg of 3-methylcholanthrene. A highly significant incidence of mesothelioma (3.8%) was noted in 159 rats treated with asbestos alone, as compared with 0.1% in 1,417 control rats. Additional treatment with radiation or 3-methylcholanthrene increased this incidence to 11.8% and 25.5%, respectively, the latter increase alone being significant at the .01 level of probability.
Another interesting study is called, Role of oxygen derivatives in the cytotoxicity and DNA damage produced by asbestos on rat pleural mesothelial cells in vitro by Hang Ying Dong, Annie Buard, Annie Renier, Francoise Lvy, Laure Saint-Etienne and Marie-Claude Jaurand - Carcinogenesis (1994) 15 (6): 1251-1255. Here is an excerpt:
Abstract - The role of reactive oxygen metabolites in the toxic effects of asbestos on pleural mesothelial cells is not well defined. We exposed rat pleural mesothelial cells (RPMC) to chrysotile and crocidolite fibers (040 g/cm2) in the presence or absence of catalase and superoxide dismutase (SOD). Cell injury was measured using the colorimetric 34 (5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and DNA damage was evaluated in terms of unscheduled DNA synthesis (UDS). Catalase (100 U/ml) and SOD (250 U/ml) protected RPMC against asbestos-induced cytotoxicity and DNA damage. However, the inactivated enzymes and bovine serum albumin also showed some protection, suggesting that the effect of antioxidant enzymes may be partly related to their protein nature. These results suggest that oxygen derivatives are partly involved in the toxic effects of asbestos on cultures of RPMC. The presence of extracellular proteins may also decrease asbestos-produced toxicity by reducing the degree of RPMCfiber interaction.
We all owe a debt of gratitude to these fine researchers for their important work. If you found any of these excerpts helpful, please read the studies in their entirety.
by: Mont Wrobleski
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