TABLE 2.
Mouse Models of Arsenic-induced CVD via Drinking Water Arsenic Exposure
| Reference | Mouse strain | Arsenic exposure and level | End point assayed and outcome |
| Bunderson et al. (2004) | ApoE, LDLr double knockout | Drinking water, 5.7 mg/l, 18 weeks | Increased atherosclerotic plaque stenosis in innominate artery |
| Simeonova et al. (2003) | ApoE-knockout | Drinking water, 11.4 or 57 mg/l, 24 weeks | Increased aortic lesions |
| Srivastava et al. (2007) | ApoE-knockout | Transplacental in drinking water, 49 mg/l, gestational days 8–18 | Increased fatty streak lesions in aortic arch and valves, defective vasorelaxation response at age 10 weeks |
| Straub et al. (2007a,b) | C57Bl/6 | Drinking water, 250 μg/l, 5 weeks | Liver sinusoidal capillarization, angiogenesis in liver bile ducts, decreased lumen in hepatic arterioles, gain in sinusoidal endothelial cell caveolin and caveolae |
| Straub et al. (2008) | C57Bl/6 p47phox knockout | Drinking water, 10–250 μg/l, 2 weeks | Liver sinusoidal capillarization, loss of modified albumin scavenging, protein nitration, oxidant generation, absence of arsenic-induced effects in knockout |