An evaluation of Ciprofloxacin toxicity in the neonatal minipig

Abstract

Sulfur dioxide (SO2) is a common air pollutant, and inhaled SO2 in airway epithelium easily forms its soluble derivatives in vivo (bisulfite and sulfite), which are toxic to the respiratory system and related to the exacerbation of asthma. In order to study the possible asthmatic molecular mechanism of SO2 and its derivatives, the dose-response and time-response relationships of SO2 derivatives on gene expressions of some asthma-related genes in human bronchial epithelial cells (BEP2D) were investigated. The mRNA and protein levels of EGF, EGFR, ICAM-1 and COX-2 were analyzed in BEP2D cells using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, radio-immunoassay (RIA) method and Western blot analysis, respectively. The results showed that SO2 derivatives caused the dose-dependent inductive expressions of four gene mRNA and protein in BEP2D cells. Moreover, SO2 derivatives significantly increased the mRNA and protein levels at 0, 0.5, 1, 4 and 24 h post-exposure, along with the highest inductions at 0.5 h post-exposure for EGFR and COX-2 and at 4 h post-exposure for EGF and ICAM-1. It was suggested that SO2 derivatives could increase the expressions of EGF, EGFR, ICAM-1 and COX-2 on the transcription and translation levels in BEP2D cells, and result in mucus over-production and inflammation responses. This might be one of the possible mechanisms that SO2 aggravates asthma disease.