cytochrome-c-t and tungsten-carbide

In this study, apoptosis and related signaling induced by WC-Co nanoparticles were investigated in JB6 cells and rat lung macrophages. Electron spin resonance (ESR) and fluorescent staining indicated that both WC-Co nanoparticles and fine particles stimulated reactive oxygen species (ROS) generation. Catalase exhibited an inhibitory effect on WC-Co nanoparticle-induced ROS as well as mitochondrial membrane permeability damage. Further study indicated that WC-Co nanoparticles elicited higher cytotoxicity and apoptotic induction than fine particles. Western blot analysis showed activation of proapoptotic factors including Fas, Fas-associated protein with death domain (FADD), caspase 3, 8 and 9, BID and BAX. In addition, both cytochrome c and apoptosis-inducing factor (AIF) were upregulated and released from mitochondria to the cytoplasm. Our findings demonstrate that, on a mass basis, WC-Co nanoparticles exhibit higher cytotoxicity and apoptotic induction than fine particles. Apoptosis induced by WC-Co nanoparticles and fine particles involves both extrinsic and intrinsic apoptosis pathways.

Topics: Air Pollutants, Occupational; Animals; Apoptosis; Apoptosis Inducing Factor; Apoptosis Regulatory Proteins; Carcinogens; Caspases; Cell Line; Cell Survival; Cobalt; Cytochromes c; fas Receptor; Lung; Macrophages; Mice; Mitochondrial Membranes; Particle Size; Permeability; Rats; Reactive Oxygen Species; Surface Properties; Tungsten Compounds