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Inhibition of cell apoptosis is an increasingly important factor in modulating airway inflammation in asthma, which is related to environmental pollutants. To investigate the effects of sulfur dioxide (SO2) on the mRNA and protein expressions of apoptosis-related genes in lungs from asthmatic rats, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (2 ppm) inhalation alone or together. Examinations were performed 24 h after the last treatment. The mRNA and protein levels of p53, bax, and bcl-2 were analyzed in lungs using real-time reverse transcription-polymerase chain reaction (RT-PCR) assay and Western blot analysis, respectively. The results indicated that increases of bcl-2 or decreases of p53 and bax mRNA and protein levels were not significant in lungs of rats exposed to SO2 alone, compared with controls, but elevated or reduced levels of these genes appeared in lungs of asthmatic rats exposed to SO2 plus OVA, compared with controls, suggesting that SO2 exposure could result in OVA-induced increases or decreases of transcription and translation levels of these apoptosis-related genes in rat lungs, and may have relations to airway inflammation in asthma. The regulation mechanism of apoptosis in asthma disease exposure to SO2 needs further study. [ABSTRACT FROM AUTHOR]

To study whether sulfur dioxide (SO 2 ) can enter into the different organs of mice exposed to SO 2 , the sulfite contents in brains, hearts, and lungs from male mice were determined by high-performance liquid chromatography with fluorescence detection (HPLC-FD). After reduction and precolumn derivation of tissue homogenates of brains, hearts, and lungs from mice, the mixture was centrifuged, and 5µl of the resulting supernatant was directly injected into HPLC; the mobile phase consisted of methanol–phosphoric acid (12:88, v/v), and for the fluorescence detection ? EX 392 nm and? EM —479 nm were used. The standard curve was linear in the range from 0.126 µg/ml to 126 µg/ml; the minimal detectable concentration was 0.04µg/ml (S/N = 3), the average methodological recoveries were from 97% to 101%, and the within-day and between-day precisions were less than 9%. These results showed that sulfite contents in all organs tested from mice in the SO 2 -exposed groups were significantly increased (p .92) compared with the control groups. These results indicated SO 2 could transform into sulfite in vivo after inhalation, and could distribute into lung and other organs such as brain and heart. These results offered a support for the viewpoint that SO 2 is a systemic toxic agent. [ABSTRACT FROM AUTHOR]