Asbestos surface provides a niche for oxidative modification.

摘要: Asbestos is a potent carcinogen associated with increased risks of malignant mesothelioma and lung cancer in humans. Although the mechanism carcinogenesis remains elusive, physicochemical characteristics asbestos play role progression asbestos-induced diseases. Among these characteristics, high capacity to adsorb accommodate biomolecules on its abundant surface area has been linked cellular genetic toxicity. Several previous studies identified asbestos-interacting proteins. Here, use matrix-assisted laser desorption ionization-time flight mass spectrometry, we systematically proteins from various lysates that adsorbed commercially used classified them into following groups: chromatin/nucleotide/RNA-binding proteins, ribosomal cytoprotective cytoskeleton-associated histones hemoglobin. The surfaces crocidolite amosite, two iron-rich types asbestos, caused more protein scissions oxidative modifications than chrysotile by situ-generated 4-hydroxy-2-nonenal. In contrast, confirmed intense hemolytic activity found hemoglobin attached chrysotile, but not silica, can work as catalyst induce DNA damage. This process generates 8-hydroxy-2'-deoxyguanosine thus corroborates involvement iron carcinogenicity chrysotile. evidence demonstrates all three specific providing niche for modification via catalytic iron. Therefore, considering affinity histones/DNA internalization mesothelial cells, our results suggest novel hypothetical causing alterations during carcinogenesis.