Traffic-Related Emissions Induce Angiotensin II-Dependent Oxidative Stress in the Hippocampus of ApoE-Null Male Mice

This study tested the hypothesis that exposure to traffic-generated air pollution (MVE) in apolipoprotein null (ApoE-/-) mice leads to increased oxidative stress and amyloid processing, associated with increased renin-angiotensin system (RAS) signaling. Methods: Male ApoE-/- mice (6-8 weeks old) on a high-fat diet were treated with either an ACE inhibitor (captopril, 4 mg/kg/day) or water and exposed to filtered air (FA) or MVE (200µg PM/m³) for 30 days. Real-time qPCR was used to analyze cerebral endpoints, double immunofluorescence to analyze protein expression in the CA1 region of the hippocampus, and an ELISA to quantify plasma angiotensin II levels.