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. 2016 Oct 6;7(10):e2397. doi: 10.1038/cddis.2016.299

Figure 3.

Figure 3

High levels of ROS in TCS embryos and prevention of craniofacial malformation through the pharmacological suppression of ROS. (a) Level of ROS measured in control (STD), TRA and TRA+ATGTp53 48 hpf embryos. Values are expressed as the mean±S.E.M. (n=42). **P<0.01 versus STD; NS= non-significant P>0.05 (t-test) AU: arbitrary units. (b) Frequencies of Normal, Mild and Severe phenotypes (see Results section) in controls (STD, n=51), TRA (n=79) and TRA-larvae incubated in the presence of NAC (TRA+NAC, n=52). **P<0.01 ***P<0.001 versus STD; ##P<0.01 versus TRA (chi-square test). (c) Acridine Orange staining in vivo performed in 24 hpf embryos (see Figure 2c for representative photos of normal (+), intermediate (++) or extensive (+++) cephalic cell death). The bar graph shows the distribution of each phenotype among the groups (STD, TRA and TRA+NAC embryos). n=25 embryos. ***P<0.001 versus STD; NS=non-significant P>0.05 (chi-square test). (d) Western blotting showing the Tp53 abundance in STD, TRA and TRA+NAC 24 hpf embryos. Molecular weight markers are shown at the right. Actin was analyzed as a loading control. The graph shows the densitometric quantification of western blotting band (normalization of Tp53 signal with respect to Actin). Bars represent mean of relative abundance and S.E.M., n=3, *P<0.05 NS,non-significant P>0.05 (Mann–Whitney test)