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Cognitive Function in Prepubertal Children with Obstructive Sleep Apnea: A Modifying Role for NADPH Oxidase p22 Subunit Gene Polymorphisms?

机译:青春期前阻塞性睡眠呼吸暂停患儿的认知功能:NADPH氧化酶p22亚基基因多态性的修饰作用?

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摘要

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. Antioxid. Redox Signal. 16, 171–177.
机译:小儿阻塞性睡眠呼吸暂停(OSA)可能会导致神经认知功能障碍,但并非所有人都受到影响。 OSA患儿与对照组之间p22phox亚基中NADPH氧化酶(NOX)多态性的频率相似,但rs6520785和rs4673除外,后者在有缺陷的OSA患儿中的频率明显高于有缺陷的患儿(p <0.02)。同样,在没有认知缺陷的儿童中,尤其是在具有rs4673多态性的儿童中,8-羟基脱氧鸟嘌呤的尿液水平和NOX活性较低。因此,NOX基因或其功能亚基内的多态性可解释儿童OSA相关认知功能缺陷方差的重要组成部分。抗氧化。氧化还原信号。 16,171–177。

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