Scandinavian Journal of Immunology · 2005 · 34 citations · 17 references
Life SciencesCell BiologyImmunologyApoptosisImmunopathologyMitochondrial BiologyApoptosis In Immune CellsIntrinsic Apoptotic PathwayMitochondrial DysfunctionMitochondrial ToxicologyReactive Oxygen SpeciesApoptotic ResponseMitochondrial Apoptosis PathwaysMitochondrial Apoptotic SignalingMitochondrial Pathway Of ApoptosisMitochondrial PathwaysReactive Oxygen Species GenerationReactive Oxygen Species InjuryReactive Oxygen Species-induced Apoptosis
To clarify the effects of silica and silicates on cellular features of lymphocytes, a human T-lymphotropic virus type-1-immortalized polyclonal T-cell line, MT-2, was exposed to various concentrations of chrysotile-A, an asbestos classified as silicate. MT-2 cells underwent apoptosis in a dose- and time-dependent manner. The mitochondrial apoptotic pathway was activated during chrysotile-A-induced apoptosis of MT-2 cells, because of the phosphorylation of JNK and p38, increase of BAX and release of cytochrome-c from mitochondria to cytoplasma. In addition, anti-oxidants such as hydroxyl-radical excluders and capturers of superoxide and inhibitors of superoxide production effectively reduced the size of the apoptotic fraction in MT-2 cells cultured with chrysotile-A. These results indicate that the activation of reactive oxygen species may play a central role in asbestos-induced T-cell apoptosis, and anti-oxidants may help to prevent complications of pneumoconiosis.
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Polyclonal human T-cell activation by silicate in vitro.
A Ueki, M Yamaguchi, Hiroaki Ueki et al. · PubMed · 1994 · 90 citations