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Fig. 3
Overview of oxidative stress in developing tissues. Following chemical exposure, changes to cellular metabolism, mitochondrial kinetics or the bio-
activation of xenobiotics into reactive metabolites can promote an increase in ROS production increases and shift intracellular redox states. Excessively
high levels of ROS generation and/or highly oxidized redox states can promote apoptosis (black arrows), but under more moderate conditions, shifts in
redox state can promote disruption to redox-sensitive cell signaling (red arrows), including important developmental pathways. Outcomes can include
structural malformations and neurobehavioral deficits. However, redox shifts can also activate compensatory pathways that are designed to restore redox
imbalance and increase ROS detoxification (green arrows). Rapid and timely restoration of redox states may serve as a means to prevent prolonged
periods of signal disruption and support normal developmental patterning.
unchanged, but increases in activity were observed in 10. Murphy MP: How mitochondria produce reactive oxygen
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degree of ROS generation, cellular macromolecules can
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cells will undergo apoptosis, whereas under lower ROS
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ferentiation of adipose-derived stem cells by triggering
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