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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAhiYmbUAABh5YRFuHt6ehtYgIzmQdHn6-1NqjjaAGkc8#_3 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAhiYmbUAABh5YRFuHt6ehtYgIzmQdHn6-1NqjjaAGkc8#_2 http://www.w3.org/ns/prov#value To study the effect of cigarette smoke on DNA damage, bronchial epithelial cells were exposed to either 5% CSE or 1 µM CPT for 24 h. The quantitative in situ TUNEL assay, in parallel with the MTT assay, was performed after 1-, 2-, 4-, 6-, and 24-h exposure. As shown in Figure 1, even 1 h of exposure to 5% CSE or CPT caused a significant increase of TUNEL-positive cells (54.9 ± 3.0% by 5% CSE and 31.2 ± 2.2% by CPT, respectively, P < 0.05 compared with control of 16.2 ± 0.3%, Figure 1A). TUNEL-positive cells gradually increased to nearly 90% in both 5% CSE- and CPT-treated groups as a function of time, although the 5% CSE effect was stronger than 1 µM CPT during the first 4 h. Cell viability as assessed by MTT, however, was not affected by 5% CSE but was significantly reduced by CPT at 6 h (100.3 ± 3.3% versus 61.3 ± 5.5% of control, P < 0.05) and at 24 h (103.2 ± 7.6% versus 26.6 ± 1.9% of control, P < 0.05; Figure 1B). 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