The new threat of mesothelioma, the asbestos from Nonoccupational

The new threat of mesothelioma, the asbestos from Nonoccupational

The development of asbestos related diseases in workers has been closely studied for some time. However, there is a new wave of mesothelioma cases from the spouses of workers who were exposed to this hazardous material emerging markets. An important study is called, "Asbestos-related diseases of Household Exposure" by Gary R. Epler, Muiris X. Fitz Gerald, Edward A. Gaensler, Charles B. Carrington - Breathing 1980 39:229-240. Here is an excerpt: "Abstract - The importance of non-occupational asbestos was emphasized recently in order to illustrate this problem, we report four people with asbestos-related disease from household exposure There were 2 women of asbestos workers who are their husbands.." Cleaned Workwear .

 A developed mesothelioma and other plaques, calcification, benign asbestos pleural effusion and subpleural parenchymal fibrosis. Two men were as children exposed while playing in a basement room that was also used for their father's muffler repair business. . At the age 27 and 33, she had pleura and diaphragm calcification "Another study investigation is called value," Asbestos induces apoptosis in human alveolar macrophages "by Hamilton RF, Iyer LL and A. Holian - Department of Internal Medicine, University of Texas Medical School, Houston 77030, USA Am J Physiol Lung Cell Mol Physiol 271:. L813-L819, 1996 Here is an excerpt:. "Asbestos is a group of fibrous minerals in the development of various lung diseases, including fibrosis (asbestosis), cancer, and malignant mesothelioma involved . Although major health risks in occupationally exposed persons exist, low-level exposure to asbestos may still lead to health problems. 

The mechanism by which asbestos causes lung disease is not clear, however, was proposed that alveolar macrophages (AM) include. We suggest that asbestos apoptosis of AM, leading to the development of an inflammatory condition. In this study, we have two forms of asbestos chrysotile (CHR) and crocidolite (CRO), examined along with a control fiber to wollastonite (WOL), characterize their relative cytotoxicity and the ability to stimulate apoptosis in vitro. AM were cultured for 24 h with these particles and examined for cell viability (trypan blue exclusion) and apoptosis (morphology, levels of cytosolic oligonucleosomal DNA fragments and DNA ladder). In the absence of a decrease in the viability of the cells both produced CHR CRO and changes in cell morphology. Apoptosis In addition, levels of cytoplasmic oligonucleosomal DNA (Cell Death Detection enzyme-linked immunosorbent assay) clearly CHR (3-25 micrograms / ml) and CRO (25-75 micrograms / ml) in a dose-dependent manner, improved (a process that was inhibitable by 10 microM Z-Val-Ala-Asp fluoromethyl ketone, an interleukin converting enzyme inhibitor). 

In contrast, WOL generated (up to 400 micrograms / ml), no significant DNA fragmentation in a 24-hour culture. Neither CHR CRO caused DNA ladder formation in 24-h cell cultures. However, in 48-h cell cultures both CHR and cell-CRO exposed, but not WOL, characteristic resulted in the formation of DNA ladders apoptosis. In summary, these results suggest that, in contrast nonfibrogenic particles, low doses of asbestos fibers apoptosis in cultured human cause clock which may be an early step in the development of lung fibrosis. "A third study is called," Iron mobilization from crocidolite greatly enhanced crocidolite-dependent formation of DNA single strand breaks in DNA øX174 RFI "by Loren G. Lund and Ann E. Aust - Department of Chemistry and Biochemistry, Utah State University, Logan , UT 84322-0300, United States Here is an excerpt:. "the ability of iron with asbestos to catalyze damage to øX174 RFI DNA was assigned to identify and mobilize iron from asbestos.

 Asbestos (1 mg / ml), suspended for 30 min in 50 mM NaCl with 0.5 ug øX174 RFI DNA, pH 7.5, does not catalyze detectable amounts of DNA single strand breaks (SSB). However, the addition ofo ascorbate (1 mM) in 19, 26, 7, or 8% resulted in DNA with SSB for crocidolite, amosite, chrysotile or tremolite respectively. The proportion of DNA with SSB was induced by any form of asbestos related directly to its iron content. Receiving desferrioxamine B which binds Fe (III), whereby it redox inactive, completely inhibited the formation of asbestos-dependent DNA SSB, suggesting that iron was responsible for catalyzing the formation of DNA-SSB. Mobilization of Fe (II) of crocidolite of citrate, EDTA or out nitrikrtriacetate (1 mM) in the absence of ascorbate in 15, 33 or 63% with DNA are SSB. This activity has been be completely compounds OH scavengers, ie mannitol, 5, 5-dimethyl-l-N-oxide or PYROLINE salicylate (100 mm). Preincubation of crocidolite with citrate (1 mM) for 24 h resulted in mobilization of 52 uM iron and increased ascorbate-dependent induction of DNA SSB compared to crocidolite was preincubated without citrate.

 Iron full responsibility for crocidolite-dependent formation of DNA SSB by complete inhibition with desferrioxamine B. was mobilized by citrate Thus occupied, the results of the present study strongly suggest that iron was responsible for the asbestos-dependent generation of oxygen radicals, which resulted in the formation of DNA SSB. Mobilization of iron by chelators, by redox cycling, greatly enhanced crocidolite-dependent formation of DNA SSB followed. Thus, mobilization of iron in vivo by low mol. Weight chelators can to the increased production of reactive oxygen species, which cause damage to biomolecules such as DNA. "If you found any of these excerpts, please read them in their entirety, we all owe a debt of gratitude to these researchers.