Fig. 1.

Particulate matter (aerodynamic diameter <2.5 μm, PM_2.5) particles are retained intracellularly and induces oxidative stress in vivo. A and B: transmission electron micrographs of lung and liver macrophages from the mice exposed to PM_2.5 or filtered air (FA) for 10 wk. E, ER; M, mitochondria. C: dihydroethidium (DHE) staining of liver tissue sections from the mice exposed to FA or PM_2.5. Frozen liver tissue sections were stained with DHE (10 μmol/l). The oxidative red fluorescence (Texas red) was detected by a Zeiss fluorescence microscope. D: DHE signals were quantified by counting the number of positive-stained nuclei in 8 random fields. Microscopic interference contrast was used to exclude positive signals from noncell origin. The percentages of DHE-positive nuclei (compared with total nuclei) were shown. Data are shown as means ± SE for 6 animals per group. **P < 0.01. P values are shown for statistically significant differences. E: quantitative real-time RT-PCR analysis of the expression of mRNAs encoding glutathione peroxidase-1 (Gpx-1), heme oxygenase-1 (HO-1), superoxide dismutase-1 (SOD1), and SOD2 in the lung tissue of the mice exposed to FA or PM_2.5. Fold changes of mRNA levels were determined after normalization to internal control β-actin RNA levels. For each comparison group, the mRNA level of one FA-exposed mouse was defined as 1 and was used to calculate the fold changes of mRNA levels for the other mice. Each bar denotes the means ± SE (n = 6 mice/group). **P < 0.01.