The ability of mineral dusts and fibres to initiate lipid peroxidation. Part II: relationship to different particle-induced pathological effects

Abstract

Exposure to pathogenic mineral dusts and fibres is associated with pulmonary changes including fibrosis and cancer. Investigations into aetiological mechanisms of these diseases have identified modifications in specific macromolecules as well as changes in certain early processes, which have preceded fibrosis and cancer. Peroxidation of lipids is one such modification, which is observed following exposure to mineral dusts and fibres. Their ability to initiate lipid peroxidation and the parameters that determine this ability have recently been reviewed. Part II of this review examines the relationship between the capacity of mineral dusts and fibres to initiate lipid peroxidation and a number of pathological changes they produce. The oxidative modification of polyunsaturated fatty acids is a major contributor to membrane damage in cells and has been implicated in a great variety of pathological processes. In most pathological conditions where an induction of lipid peroxidation is observed it is assumed to be the consequence of disease, without further establishing if the induction of lipid peroxidation may have preceded or accompanied the disease. In the great majority of instances, however, despite the difficulty in proving this association, a causal relationship between lipid peroxidation and disease cannot be ruled out.

Effects of natural acids on surface properties of asbestos minerals and kaolinite

“…[1] Although there is considerable debate and controversy, the literature suggests that there are several factors that influence the potential health effects of these naturally occurring minerals, such as: type of mineral, surface area, length of fibre, atomic structural arrangements, length of time of exposure, oxidative potential (reactive oxygen species -ROS) and surface adherence. [1][2][3][4] It has been suggested that molecular structure determines the potential toxicity of soluble compounds; however, mineral particles' shape, chemical characteristics, size, surface roughness, exposure of crystal planes and surface functional groups all contribute to the ultimate toxicity. [1 , 5] Natural minerals are not thermodynamically stable when exposed to the terrestrial/atmospheric environment and are chemically attacked by naturally occurring acids that alter their chemical structure and thus their chemical reactions.…”

Role of 4‐hydroxy‐2,3‐nonenal in the pathogenesis of fibrosis

“…Among all profibrogenic molecules, TGFβ1 is most clearly linked to the development of fibrosis during the course of many diseases, including cirrhosis, chronic hepatitis, glomerulonephritis, diabetic nephropathy, atherosclerosis, scleroderma and pulmonary fibrosis [2,4,5,13,28].…”