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Induction of Apoptosis by Tungsten Carbide‐Cobalt Nanoparticles in JB6 Cells Involves ROS Generation through both ‘Extrinsic’ and ‘Intrinsic’ Apoptotic Pathways
Author(s) -
Ding Min,
Zhao Jinshun,
Bowman Linda,
Leonard Stephen,
Castranova Vincent
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.798.26
Subject(s) - reactive oxygen species , apoptosis , cytotoxicity , cytochrome c , chemistry , biophysics , microbiology and biotechnology , materials science , biochemistry , biology , in vitro
Tungsten Carbide‐Cobalt (WC‐Co) nanoparticle composites have wide applications because of their hardness and toughness. In this study, apoptosis and related signaling induced by WC‐Co were investigated. Electron spin resonance (ESR) and fluorescent staining indicated that both WC‐Co nano‐ and fine particles stimulated reactive oxygen species (ROS) generation. Catalase inhibit WC‐Co‐induced ROS as well as mitochondrial membrane permeability damage, indicating that H2O2 may play an important role in the cytotoxicity induced by WC‐Co. Further studies indicated that WC‐Co nanoparticles elicited a higher cytotoxicity and apoptotic induction than fine particles. Western‐blot analysis showed an activation of proapoptotic factors including Fas, FADD, caspase 3, 8 and 9, BID, and BAX. Lamin A and beta‐actin were cleaved. Interestingly, WC‐Co particles also induced Bcl‐2, an anti‐apoptotic factor, up‐regulation. In addition, both cytochrome c and AIF were up‐regulated and released from mitochondria to the cytoplasm. The results demonstrate that apoptosis induced by WC‐Co involve both ‘extrinsic’ and ‘intrinsic’ apoptotic pathways and nanoparticles exhibit higher cytotoxicity and apoptotic induction than fine particles.