CRISTINA LAURA HOMEGHIU, GABRIELA BUCATA, ADELA BONOIU, CRISTINA STAN, VALENTINA MITRAN, ANIŞOARA CÎMPEAN, DANA IORDĂCHESCU
Research Center for Biochemistry and Molecular Biology, University of Bucharest, 93–95, Splaiul Independenţei, Bucharest, Romania
Abstract. The present study belongs to a larger research concerning the elaboration of a cellular model to study the pathogenesis of pulmonary fibrosis that consist of human embryonic lung fibroblasts (HELFs) treated in combination with CdCl2 and TGF-β1. Exposure of HELFs at Cd doses higher than 200 μM led to an increased intracellular reactive oxygen species (ROS) production, the releasing of TBARS substances in the culture medium as well as internucleosomal DNA fragmentation, in a dose-dependent manner. Treatment of cells with 20 ng/ml TGF-β1, for 24 h, increased the production of ROS approximately 4-fold over the control values; without to induce an oxidative stress that suggest that ROS act as second messenger in signal transduction pathways. In these experimental conditions TGF-β1 does not induce HLEF apoptosis and stimulates cell proliferation. In the cells co-treated with 50 μM CdCl2 and 20 ng/ml TGF-β1, the level of intracellular ROS was increased with 56.8% compared with control HELFs and decreased with 61.3% with regard to the cells incubated only with TGF-β1, suggesting an antioxidant protective effect of this dose of CdCl2. The combined treatment did not lead to an oxidative stress but increased with 45% the apoptotic process showing a clear association between Cd exposure and TGF-β1-induced responses.
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