Table 3.

Developmental neurotoxins targeting NADPH oxidase.

Chemical	Exposure, species	Toxicities on NOX in the developing brain	Other findings in pups	References
Sevoflurane	Mouse pups at PND6 were anesthetized with 3% sevoflurane in 40% oxygen for 6 h	p22phox protein expression was increased in the brain shortly after exposure	ROS, cytochrome c, and cleaved caspase-3 were increased in the brain shortly after exposure. Abnormal freezing behavior was observed at 11-13 weeks of age. These toxicities were suppressed by cotreatment with the NOX inhibitor	[78]
Sevoflurane	Mouse pups were anesthetized with 3% sevoflurane in 40% oxygen for 2 h daily from PND6 to PND8	NOX2 protein expression was increased in FC and HC shortly after exposure	Apoptosis was increased in the brain shortly after exposure. Abnormal freezing behavior and the impairments of spatial learning and memory were observed at 9-11 weeks of age	[77]
Ethanol	Pregnant mice at GD8 were injected IP with ethanol (12 g/kg)	The mRNA expressions of Duox2, Noxa1, and Noxo1 were increased in the brains on GD18	The mRNA expressions of Noxa1 and p67phox were increased in the placenta and liver, respectively, on GD18	[81]
Ethanol	Pregnant mice at GD9 were injected IP with ethanol (2.9 g/kg)	The mRNA expressions of Duox1, Noxa1, Noxo1, p22phox, p67phox, and Rac1 were increased in the brains shortly after exposure	NOX activity, ROS generation, oxidative DNA damage, and apoptosis were increased in the brains shortly after exposure. These toxicities were suppressed by cotreatment with the NOX inhibitor	[82]

GD: gestational day; PND: postnatal day; FC: frontal cortex; HC: hippocampus; IP: intraperitoneal.