Marginal Increases in Mean Tail Moments and Mesothelioma Cells
We must focus our energy on finding a cure to Mesothelioma
. It is a terrible disease and takes the lives of thousands every year. One interesting study is called, "DNA single strand breaks induced by asbestos fibers in human pleural mesothelial cells in vitro" by T. Ollikainen, K. Linnainmaa, and V.L. Kinnula - Environmental and Molecular Mutagenesis - Volume 33, Issue 2, pages 153160, 1999. Here is an excerpt: "Abstract - The mechanisms of the cellular effects and DNA damage caused by asbestos fibers in human mesothelial cells are not well understood. We exposed transformed human pleural mesothelial cells to 14 g/cm2 crocidolite and to 10100 ng/ml tumor necrosis factor alpha for up to 48 hr and studied the induction of DNA damage using the Comet assay. As a positive control, 100 M H2O2 was used. The DNA single strand breaks were assessed as the mean tail moments and as distributions of the tail DNA in the cell. The Comet assay showed significant but reversible increases in the mean tail moments, but not in the distribution of Comet tails in the histograms in cells exposed to 1 g/cm2 crocidolite for 6 hr. At higher concentrations of asbestos fibers all the indices in the Comet assay showed significant and irreversible change. All the doses of TNF- caused marginal increase in the mean tail moments. The mean tail moments were highest in the cells with concurrent treatment to TNF- and crocidolite. In the cells pretreated with inhibitors of antioxidant enzymes (aminotriazole for catalase and buthionine sulfoximine for -glutamylcysteine synthetase) asbestos fibers slightly increased oxidant-related fluorescence of dichlorofluorescein (DCFH) but did not cause any further increases in the mean tail moments. This study shows that asbestos fibers cause DNA single strand breaks in human mesothelial cells. Since the inhibition of antioxidant enzymes did not have an effect on the DNA damage caused by the fibers, other mechanisms than free radicals seem to be involved in the induction of DNA damage by mineral fibers. Environ. Mol. Mutagen. 33:153160"
Another interesting study is called, "Individual asbestos exposure: smoking and mortality-a cohort study in the asbestos cement industry." By M Neuberger, M Kundi
Br J Ind Med 1990;47:615-620. Here is an excerpt: "Abstract - A historical prospective cohort study comprised all persons employed from 1950 to 1981 for at least three years in the oldest asbestos cement factory in the world. From 2816 persons eligible for the study, record based estimates and measurements of dust and fibres and histories of smoking based on interviews were used to calculate individual exposures over time. After observation of 51,218 person-years and registration of 540 deaths, underlying causes of death for this cohort were compared with those for the regional population on the basis of death certificates. Deaths from lung cancer in asbestos cement workers were higher (standard mortality ratio (SMR) 1.7), but after adjustment for age and sex specific smoking habits this was not significant (SMR 1.04). The study had a probability of greater than 92% of detecting a smoking adjusted SMR of 1.5 or more. Using the best available evidence (including necropsy records) 52 deaths were assigned to lung cancer and five to mesothelioma. Life table analyses confirmed the predominant influence of smoking on lung cancer. Mesothelioma was associated with the use of crocidolite in pipe production. From present working conditions with much lower concentrations of chrysotile and no crocidolite."
Another study is called, "Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin." By I M Hill, P H Beswick, K Donaldson - Occup Environ Med 1995;52:92-96. Here is an excerpt: "Abstract Objective -To investigate the ability of short and long fibre samples of amosite asbestos to stimulate superoxide production in isolated rat alveolar macrophages, and to determine how opsonisation with rat immunoglobulin might modify this response. METHODS--Macrophages were isolated from rat lung by bronchoalveolar lavage and challenged with both opsonised and non-opsonised long and short fibres of amosite asbestos. Release of superoxide anions was measured by the spectrophotometric reduction of cytochrome c, in the presence and absence of superoxide dismutase. RESULTS--Both long and short fibre samples of amosite asbestos without opsonisation were ineffective in stimulating isolated rat alveolar macrophages to release superoxide anions in vitro. After opsonisation with immunoglobulin, however, a dramatic enhancement of release of superoxide anion was seen with long fibres, but not short, which confirms the importance of fibre length in mediating biological effects. The increased biological activity of the long fibre sample is explained by increased binding of the opsonin to the fibre surface as, at equal mass, the long fibres bound threefold more immunoglobulin than the short fibres. CONCLUSION--Opsonisation is an important factor in modulation of the biological activity of fibres at the cellular level. Differences in binding of opsonin to samples of fibre previously considered to be identical apart from length, suggest that surface reactivity needs to be taken into account when fibres are compared. Binding of biological molecules, in vivo, may thus be an important modifying factor in the pathological processes initiated by fibres."
We all owe a debt of gratitude to these fine researchers for their hard work and dedication. If you found any of these excerpts interesting, please read the studies in their entirety.
Marginal Increases in Mean Tail Moments and Mesothelioma Cells
By: Montwrobleski77
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