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Fig. 4 | Particle and Fibre Toxicology

Fig. 4

From: ROS promote epigenetic remodeling and cardiac dysfunction in offspring following maternal engineered nanomaterial (ENM) exposure

Fig. 4

Mechanisms governing cardiac and mitochondrial dysfunction following maternal nano-TiO2 inhalation exposure. a Hydrogen peroxide (H2O2) concentration in fetal (n = 6 Sham, n = 5 Ex) and young adult (n = 7 Sham, n = 5 Ex) animals, normalized to protein content. b Hif1α activity was measured in fetal (n = 4 Sham, n = 5 Ex) heart and normalized to protein content. c Dnmt1 protein expression was assessed in fetal (n = 4 Sham, n = 5 Ex) heart and normalized using anti-Gapdh primary antibody. d Global 5-methylcytosine (5-mC) DNA methylation levels were evaluated in fetal (n = 6 Sham, n = 5 Ex) hearts, normalized to DNA concentration. e GPx4 levels were assessed in fetal (n = 4 Sham, n = 4 Ex) and (f) young adult (n = 4 Sham, n = 5 Ex) animals and normalized using anti-Gapdh primary antibody. Sham = control filtered air exposed, Ex = nano-TiO2 exposed, Maternal (M) = 12-week old pregnant dams, Fetal (F) = GD (15), Young Adult (YA) = 11 weeks, Hif1α = Hypoxia-inducible factor 1-alpha, Dnmt1 = DNA (cytosine-5)-methyltransferase 1, GPx4 = Glutathione peroxidase 4. All data are presented as the mean ± standard error of the mean (SEM). * = P ≤ 0.05, ** = P ≤ 0.01, *** = P ≤ 0.001 for Ex vs. Sham

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