Glutathione Facts

Oxygen radicals in mesothelial cells after exposure to amosite

The history of the disease Mesothelioma is a tragedy for many reasons. First, it is preventable. An interesting study called, "Studies on the role of oxygen radicals in asbestos-induced cytopathology crop human lung mesothelial cells "by Edward W. Gabriel, Gerald M. Rosen, Roland C. Grafstrom, Karyn E. Strauss and Curtis C. Harris 1 – Carcinogenesis (1986) 7 (7): 1161-1164. Here's an excerpt: "Abstract – The possible role of oxygen radicals in mediating the pathological effects of asbestos-cyto cells was studied mesothelial cells in culture. Measurements of electron paramagnetic resonance of intact cells using the spin trap 5, 5-dimethyl-1-pyrroline-l-oxide did not detect any increased oxygen radicals in mesothelial cells after exposure to amosite asbestos, although oxygen radicals were easily detected in cells exposed to menadione, an uncoupler of oxidation and reduction. cellular thiol levels were reduced after exposure to menadione, but were not affected by exposure to asbestos. In addition to the culture media of the free radical scavengers superoxide dismutase, Reduced Glutathione, N-acetylcysteine or D-α-tocopherol had no effect on the cytoplasm dose-dependent toxicity of amosite fibers. Furthermore, exposure of mesothelial cells was amosite fibers in a significant increase in the level of DNA single-strand breaks. These results suggest that for cultured human mesothelial cells, oxygen free radicals are important mediators of the cytopathic effect of asbestos. "

Another interesting study called "asbestos-related cancers in the refinery Ontario and the petrochemical industry "by Murray M. Finkelstein, PhD, MDCM – American Journal of Industrial Medicine – Volume 30, Number 5, pages 610-615, November 1996 – Here's an excerpt:. Summary – Asbestos has been used extensively in the refining and petrochemical sector mesothelioma has occurred among maintenance workers, The hypothesis was that mesothelioma is a marker of exposures that may increase the risk of lung cancer. A study of case-control death certificate-based lung cancer and mesothelioma from 1980 to 1992 was conducted in a county of Ontario with a significant presence in these industries. Each of the 17 men who died from mesothelioma and 424 with lung cancer were compared with controls who died of other causes. Labor and Industry certificates death camps were summarized.

The employment as a maintenance worker in the refining and petrochemical sector was associated with an increased risk of mesothelioma (odds ratio: 24.5, 90% confidence interval 3.1 to 102). The risk of lung cancer among petrochemical workers, compared with other workers in the county, was 0.88. In an internal comparison maintenance employees with other blue-collar workers in the refining and petrochemical sector, the odds ratio for lung cancer was 1.73 (90% confidence interval confidence from 0.83 to 3.6). This finding is consistent with no difference in risk between maintenance and other employees, but also supports the study power is too low to reach statistical significance. The hypothesis of an increased risk of lung cancer could be discussed further with studies nested case-control in existing cohorts. Meanwhile, it would be prudent to strengthen adherence to the measures of control of asbestos at the refinery and petrochemical sector. "

Another study called, "Asbestos causes 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's an excerpt: "
To test the hypothesis that cell injury mediated by asbestos is mediated through an oxidant-dependent mitochondrial pathway, isolated mesothelial cells were examined by mitochondrial DNA damage as determined by quantitative PCR. Mitochondrial DNA damage occurred four times lower concentrations of crocidolite asbestos in comparison with the concentrations required for nuclear DNA damage. DNA damage by asbestos was preceded by stress oxidant, as shown by confocal laser microscopy with MitoTracker Green FM and the oxidant probe Redox Sensor Red CC-1. These events were associated with dose-dependent decreases mRNA levels in steady state of cytochrome c oxidase subunit 3 (CoIII) and NADH dehydrogenase 5. Subsequently, dose-dependent decreases in the production of formazan, an indication of mitochondrial dysfunction, increased mRNA expression of pro-and antiapoptotic genes, and increased number of cells apoptotic were observed in mesothelial cells exposed to asbestos. The possible role of mitochondria-derived pathways to apoptosis induced by asbestos was confirmed by significant reduction after pretreatment of cells with an inhibitor of caspase-9. Apoptosis was reduced in the presence of catalase. past use, HeLa cell transfected with a mitochondrial transport sequence of the target human DNA glycosylase repair enzyme 8-oxoguanine DNA to mitochondria demonstrated that apoptosis induced by asbestos has been enhanced with increased cell survival. The studies taken together indicate that mitochondria are the initial targets of asbestos DNA damage and apoptosis induced through a mechanism related oxidants. "

We all owe a debt of gratitude to these researchers for their important work fine. If you find any of these extracts help, please read the studies in their entirety.

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