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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

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

Fig. 6

Illustration of molecular pathways altered during maternal nano-TiO2 inhalation exposure and physiological ramifications. Following maternal exposure, increased ROS in fetal cardiac tissue and decreased mitochondrial ROS scavenging through GPx4 perpetuates a positive feedback-loop where increased Hif1α activity acts to transcriptionally activate Dnmt1 and ultimately increase global 5-methylcytosine levels. While ROS returns to control levels in the young adult animals, fetal insult negatively influences mitochondrial and cardiac function in maternal nano-TiO2 inhalation exposed progeny into adulthood. Maternal (M) = 12-week-old pregnant dams, Fetal (F) = GD (15), Young Adult (YA) = 11 weeks, ROS = reactive oxygen species, GPx4 = Glutathione peroxidase 4, Hif1α = Hypoxia-inducible factor 1-alpha, Dnmt1 = DNA (cytosine-5)-methyltransferase 1, Me = 5-methylcytosine

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