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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: Food Chem Toxicol. 2014 May 16;70:114–119. doi: 10.1016/j.fct.2014.05.002

Fig. 2.

Fig. 2

α-amylase inhibited strand-breaking genotoxic DNA damage induced by PLPs such as EGCG (A) and pyrogallol (B), but did not inhibit strand-breaking genotoxic DNA damage induced by the chemotherapeutic camptothecin (C) in the p53R assay. In each experiment, p53R cells were plated in triplicate and treated with various doses of each injurant for 18 h in the presence or absence of α-amylase at 50 units/ml. p53 reporter activity was measured in a luciferase assay. Luminescence was calculated relative to the untreated sample. The mean for each triplet was plotted for each treatment. Each experiment was performed three times with similar results. Data from representative experiments are shown.