of Work: Researchers in cardiovascular biology are working to identify the important cells and molecules involved in each stage of atherosclerosis, as well as the environmental and genetic factors that promote lesion formation. In vivo models that mimic the human disease or rely too heavily on in vitro systems could be misleading. Until recently, atherogenesis had been studied mainly in primates and in low density lipoprotein (LDL) receptor deficient rabbits. An inhalation study was conducted to investigate the progression and mechanism of carbon disulfide atherosclerosis in C57BL/6 mice; a model more appropriate for extrapolation to humans. New studies will focus on the use of ApoE knock out mice to address atherosclerosis hypothesis following environmental exposure.
| Sills, Robert C; Harry, G Jean; Valentine, William M et al. (2005) Interdisciplinary neurotoxicity inhalation studies: Carbon disulfide and carbonyl sulfide research in F344 rats. Toxicol Appl Pharmacol 207:245-50 |
| Lewis, J G; Graham, D G; Valentine, W M et al. (1999) Exposure of C57BL/6 mice to carbon disulfide induces early lesions of atherosclerosis and enhances arterial fatty deposits induced by a high fat diet. Toxicol Sci 49:124-32 |
