Oxygen Radicals in Mesothelial Cells after Exposure to Amosite Asbestos

The tale of Mesothelioma disease is a tragic one for many reasons

. First and foremost, it was avoidable. One interesting study is called, "Studies on the role of oxygen radicals in asbestos-induced cytopathology of cultured human lung mesothelial cells" by Edward W. Gabrielson, Gerald M. Rosen, Roland C. Grafstrom, Karyn E. Strauss and Curtis C. Harris1 - Carcinogenesis (1986) 7 (7): 1161-1164. Here is an excerpt: "Abstract - The possible role of oxygen radicals in mediating the cyto-pathologic effects of asbestos was studied using human mesothelial cells in culture. Electron paramagnetic resonance measurements of intact cells using the spin trap 5, 5-dimethyl-1-pyrroline-l-oxide failed to detect any increase in oxygen radicals in mesothelial cells after exposure to amosite asbestos, although oxygen radicals were readily detected in cells exposed to menadione, an uncoupler of oxidation reduction reactions. Cellular thiol levels were reduced after exposure to menadione, but were not affected by exposure to asbestos. Addition to the culture media of the free radical scavengers superoxide dismutase, reduced glutathione, N-acetylcysteine, or D--tocopherol had no affect on the dose-dependent cyto-toxicity of amosite fibers. Furthermore, exposure of the mesothelial cells to amosite fibers resulted in no significant increase in the level of DNA single-strand breaks. These results all suggest that for cultured human mesothelial cells, oxygen free radicals are not important mediators of the cytopathic effect of asbestos."

Another interesting study is called, "Asbestos-associated cancers in the Ontario refinery and petrochemical sector" by Murray M. Finkelstein PhD, MDCM - American Journal of Industrial Medicine - Volume 30, Issue 5, pages 610615, November 1996 Here is an excerpt: "Abstract - Asbestos has been widely used in the refinery and petrochemical sector. Mesothelioma has occurred among maintenance employees, and it was hypothesized that mesothelioma is a marker for exposures which might increase lung cancer risk. A death certificate-based case-control study of mesothelioma and lung cancer from 1980 to 1992 was conducted in an Ontario county with a substantial presence of these industries. Each of the 17 men who died of mesothelioma and 424 with lung cancer were matched with controls who died of other causes. The Job and Industry fields on the death certificates were abstracted.

Employment as a maintenance worker in the refinery and petrochemical sector was associated with an increased risk of mesothelioma (odds ratio: 24.5; 90% confidence interval 3.1102). The risk of lung cancer among petrochemical workers, in comparison with all other workers in the county, was 0.88. In an internal comparison of maintenance employees with other blue-collar workers in the refinery and petrochemical sector, the odds ratio for lung cancer was 1.73 (90% confidence interval 0.833.6). This finding is consistent with no difference in risk between maintenance and other employees, but it is also compatible with study power being too low to achieve statistical significance. The hypothesis of increased lung cancer risk could be examined more fully with nested case-control studies in existing cohorts. Meanwhile, it would be prudent to reinforce adherence to asbestos control measures in the refinery and petrochemical sector."

Another study is called, "Asbestos induces mitochondrial DNA damage and dysfunction linked to the development of apoptosis" by Arti Shukla, Michael Jung, Maria Stern, Naomi K. Fukagawa, Douglas J. Taatjes, Dennis Sawyer, Bennett Van Houten, and Brooke T. Mossman - Am J Physiol Lung Cell Mol Physiol 285 Here is an excerpt: "

To test the hypothesis that asbestos-mediated cell injury is mediated through an oxidant-dependent mitochondrial pathway, isolated mesothelial cells were examined for mitochondrial DNA damage as determined by quantitative PCR. Mitochondrial DNA damage occurred at fourfold lower concentrations of crocidolite asbestos compared with concentrations required for nuclear DNA damage. DNA damage by asbestos was preceded by oxidant stress as shown by confocal scanning laser microscopy using MitoTracker Green FM and the oxidant probe Redox Sensor Red CC-1. These events were associated with dose-related decreases in steady-state mRNA levels of cytochrome c oxidase, subunit 3 (COIII), and NADH dehydrogenase 5. Subsequently, dose-dependent decreases in formazan production, an indication of mitochondrial dysfunction, increased mRNA expression of pro- and antiapoptotic genes, and increased numbers of apoptotic cells were observed in asbestos-exposed mesothelial cells. The possible contribution of mitochondrial-derived pathways to asbestos-induced apoptosis was confirmed by its significant reduction after pretreatment of cells with a caspase-9 inhibitor. Apoptosis was decreased in the presence of catalase. Last, use of HeLa cells transfected with a mitochondrial transport sequence targeting the human DNA repair enzyme 8-oxoguanine DNA glycosylase to mitochondria demonstrated that asbestos-induced apoptosis was ameliorated with increased cell survival. Studies collectively indicate that mitochondria are initial targets of asbestos-induced DNA damage and apoptosis via an oxidant-related mechanism."

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.

Oxygen Radicals in Mesothelial Cells after Exposure to Amosite Asbestos

By: Montwrobleski77

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