A Synergistic Vascular Effect of Airborne Particulate Matter and Nickel in a Mouse Model

• DOI: 10.1093/toxsci/kft136
• Publication Date: 2013-06-21T04:16:46Z
• Authors: Zhekang Ying; Xiaohua Xu; Minjie Chen; Dongyao Liu; Minhua Zhong; Lung-chi Chen; Qinghua Sun; Sanjay Rajagopalan
• Keywords: Endothelial Dysfunction; Monocyte

Both epidemiological and empirical studies have indicated that nickel (Ni) may play an important role in PM2.5 exposure–induced adverse cardiovascular effects. However, the underlying mechanism remains unclear. In present study, we exposed mice to concentrated ambient (CAP), Ni, or coexposure both CAP + Ni a specially designed whole-body exposure system for duration of 3 months investigated their effects on vascular function, oxidative stress, inflammation. induced greater endothelial dysfunction compared with alone. decreased nitric oxide synthase (eNOS) dimers aorta, which was potentiated by CAP. alone did not reduce NOS but more effective than decreasing phosphorylation eNOS (S1177) Akt (T308). had minimal expression inflammatory genes synergized marked upregulation tumor necrosis factor-alpha monocyte chemotactic protein-1. The monomer formation cells were redox dependent as evidenced attenuation Tiron cultured cells. lipopolysaccharide, another bioactive component reducing dimerization induces through stress-dependent inhibition dimerization. Its interaction other components significantly contribute exposure.