SO(2) inhalation modulates the expression of pro-inflammatory and pro-apoptotic genes in rat heart and lung.

SO(2) is a common air pollutant, and human exposure to SO(2) has become increasingly widespread due to the combustion of fossil fuels. The epidemiological studies have linked SO(2) exposure not only with many respiratory responses, but also with cardiovascular diseases. Also, its possible toxicity has been implicated by determining oxidative stress, DNA damage and membrane channel alteration in rat heart and lung. However, its detailed mechanisms remain unclear. In the present study, rats were treated with 7, 14 and 28 mg/m(3) SO(2) for 6h/day for 7 days, and the mRNA levels of TNF-α, IL-1β, iNOS, ICAM-1, Bax and Bcl-2 and subsequent insults were determined in the heart and lung. The results indicate that SO(2) inhalation markedly elevated TNF-α and IL-1β mRNA levels and secretions, enhanced iNOS and ICAM-1 mRNA levels and the ratio of Bax/Bcl-2 in a concentration-dependent manner, and induced occurrence of apoptosis. This suggests that SO(2) inhalation induced an inflammatory response and subsequent insults via modulating pro-inflammatory and pro-apoptotic genes in the heart and lung, which contributed to the increased risk of respiratory and cardiovascular diseases.