Inhibitory effects of anti-oxidants on apoptosis of a human polyclonal T-cell line, MT-2, induced by an asbestos, chrysotile-A.
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.
Hyodoh
F
F
Department of Hygiene, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Takata-Tomokuni
A
A
Miura
Y
Y
Sakaguchi
H
H
Hatayama
T
T
Hatada
S
S
Katsuyama
H
H
Matsuo
Y
Y
Otsuki
T
T
D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D017632:Asbestos, Serpentine / Q000009:adverse effects*; D002461:Cell Line, Transformed / Q000187:drug effects / Q000502:physiology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000494:pharmacology*; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D013481:Superoxides / Q000037:antagonists & inhibitors* / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects / Q000502:physiology; D013997:Time Factors
D017632:Asbestos, Serpentine; D016166:Free Radical Scavengers; D013481:Superoxides; D004121:Dimethyl Sulfoxide