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. 2011 Apr 14;184(1):82–91. doi: 10.1164/rccm.201012-1967OC

Figure 1.

Figure 1.

Lipid peroxidation and aorta lectin-like oxidized low-density lipoprotein receptor (LOX-1) transcriptional changes in ApoE−/− mice exposed to vehicular exhaust. (A) Expression of aortic thiobarbituric acid reactive substances (TBARS) and (B) aortic LOX-1 mRNA levels in ApoE−/− mice exposed for 6 h/d for 7 days to either filtered air (FA, n = 8), gasoline engine emissions (GEE, 60 μg particulate matter [PM]/m3, n = 8), diesel engine emissions (DE, 300 μg PM/m3, n = 8), mixed engine emissions (ME, 50 μg PM/m3 GEE + 250 μg PM/m3 DE emissions, n = 8), filtered air for 50 days (FA – 50d, n = 10), or mixed engine emissions for 50 days (ME, 50 μg PM/m3 GEE + 250 μg PM/m3 DE emissions, n = 8). (C) Aorta lipid peroxidation (TBARS) levels in ApoE−/− mice exposed for 6 h/d for 50 days to either FA (n = 10), GEE (60 μg PM/m3, n = 8), DE (300 μg PM/m3, n = 8), ME-3 (300 μg PM/m3, n = 10), ME-1 (100 μg PM/m3, n = 10), ME with PM filtered (MEG, n = 10), sulfate PM (S PM, 300 μg PM/m3, n = 10), or sulfate PM + ME (300 μg PM/m3, n = 10). Note that data for the DE and GEE exhausts are derived from previous studies (16, 20) normalized to the individual control data for each exposure, presented here to provide reference for the degree of response to the combined emissions exposure. *P ≤ 0.050 compared with FA control mice for each panel.