NOX, the main regulator in oxidative stress in experimental models of phenylketonuria?
NOX, the main regulator in oxidative stress in experimental models of phenylketonuria?
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NOX，苯丙酮尿症实验模型中氧化应激的主要调节因子？
DOI：
10.1515/jpem-2012-0387
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发表时间：
2013-08
期刊：
影响因子：
--
通讯作者：
gu xuefan
中科院分区：
文献类型：
--
作者：
he yingzhong;gu xuefan
摘要目的：目的探讨苯丙酮尿症（PKU）氧化分子调控机制中烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶（NOX）在氧化还原信号整合中的作用。方法：分别从Pahenu 2-BTBR PKU和野生型小鼠获得血液样品。测定苯丙氨酸（Phe）浓度、总抗氧化能力（T-AOC）、谷胱甘肽（GSH）和丙二醛（MDA）。收集单核细胞后，进行NOX的逆转录聚合酶链反应（RT-PCR）。此外，测定单个核细胞中的NOX活性和超氧化物。结果：与对照组相比，PKU小鼠血浆Phe浓度、T-AOC和MDA含量均显著升高（p<0.01，p<0.05，p<0.01）。而PKU组GSH含量低于对照组（p<0.05）。PKU组p47 phox、p67 phox mRNA表达水平明显升高（p<0.05），而gp 91 phox mRNA表达水平无明显变化（p>0.05）。苯丙酮尿症小鼠体内NO_x活性和超氧化物歧化酶活性也明显升高（p<0.05）。结论：在PKU的氧化分子调控机制中，NOX可能参与了氧化还原信号的整合。
Abstract Aim: To reveal the role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) in the integration of the redox signal in the oxidative molecular regulation mechanism in phenylketonuria (PKU). Methods: The blood samples were obtained from Pahenu2-BTBR PKU and wild-type mice, respectively. Phe concentration, total antioxidant capacity (T-AOC), glutathione (GSH) and maleic dialdehyde (MDA) were analyzed. After collection of the mononuclear cells, reverse transcription polymerase chain reaction (RT-PCR) for NOX was performed. In addition, NOX activity and superoxide in mononuclear cells were determined. Results: Compared to the control group, Phe concentration, T-AOC and MDA were markedly increased in PKU mice (p<0.01, p<0.05, p<0.01, respectively). However, the GSH level in PKU mice was less than that in control group (p<0.05). The mRNA level of subunits of NOX included p47phox and p67phox, were increased in PKU mice (p<0.05), however, the gp91phox had no obvious change in the two groups (p>0.05). NOX activity and superoxide were also remarkably elevated in PKU mice (p<0.05). Conclusion: NOX may play an important role in the integration of the redox signal in the oxidative molecular regulation mechanism in PKU.