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. 2012 Jan 15;16(2):171-7.
doi: 10.1089/ars.2011.4189. Epub 2011 Oct 12.

Cognitive function in prepubertal children with obstructive sleep apnea: a modifying role for NADPH oxidase p22 subunit gene polymorphisms?

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Cognitive function in prepubertal children with obstructive sleep apnea: a modifying role for NADPH oxidase p22 subunit gene polymorphisms?

David Gozal et al. Antioxid Redox Signal. .

Abstract

Pediatric obstructive sleep apnea (OSA) may lead to neurocognitive dysfunction, but not in everyone affected. The frequencies of NADPH oxidase (NOX) polymorphisms in the p22phox subunit were similar between children with OSA and controls, except for rs6520785 and rs4673, the latter being significantly more frequent among the OSA children without deficits than with deficits (p<0.02). Similarly, 8-hydroxydeoxyguanine urine levels and NOX activity were lower among children without cognitive deficits and particularly among those with the rs4673 polymorphism. Thus, polymorphisms within the NOX gene or its functional subunits may account for important components of the variance in cognitive function deficits associated with OSA in children.

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Figures

FIG. 1.
FIG. 1.
Pairwise linkage disequilibrium structure and 18 SNPs of the NADPH oxidase (NOX) gene in children with obstructive sleep apnea (OSA) (right panel) and controls (left panel). No significant differences in allelic frequency emerged among the two groups except for rs4673 and rs6520785 polymorphisms.
FIG. 2.
FIG. 2.
NADPH oxidase basal activity in children with and without OSA (left upper panel), with and without cognitive deficits in the context of OSA (right upper panel), and among the latter, those with and without the p22 phox subunit single-nucleotide polymorphism rs4673 (242 C>T; lower panel).

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