Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA.
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA; Department of Neuroscience, University of Parma, Parma, Italy.
Ann Glob Health. 2016 Jan-Feb;82(1):100-10. doi: 10.1016/j.aogh.2016.01.009.
Acute and chronic exposures to widely used organophosphorus (OP) insecticides are common. Children's detoxification mechanisms are not well developed until several years after birth. The increased cases of neurodevelopmental disorders in children, together with their increased susceptibility to OP neurotoxicity cannot be explained by genetic factors alone but could be related to gene-environment interactions. Paraoxonase-1 (PON1) is an enzyme that can detoxify OPs but its catalytic efficiency for hydrolysis to certain OPs is modulated by the Q192R polymorphism. Studies with animals have provided important information on the role of PON1 in protecting against gestational and postnatal toxicity to OPs. The PON1Q192 allele is less efficient in hydrolyzing certain OPs than the PON1R192 allele. Maternal PON1 status (PON1 activity levels, the most important measurement, and functional Q192R phenotype) modulates the detrimental effects of exposure to the OP chlorpyrifos oxon on fetal brain gene expression and biomarkers of exposure. Epidemiologic studies suggest that children from mothers with lower PON1 status who were in contact with OPs during pregnancy tend to show smaller head circumference at birth and adverse effects in cognitive function during childhood. Infants and children are vulnerable to OP toxicity. The detrimental consequences of OPs on neurodevelopment can lead to future generations with permanent cognitive problems and susceptibility to develop neurodegenerative diseases. Improved methods using mass spectrometry to monitor OP-adducted biomarker proteins are needed and will be extremely helpful in early life biomonitoring, while measurement of PON1 status as a biomarker of susceptibility will help identify mothers and children highly sensitive to OPs. The use of adductomics instead of enzymatic activity assays for biomonitoring OP exposures have proved to provide several advantages, including the use of dried blood spots, which would facilitate monitoring newborn babies and children.
急性和慢性接触广泛使用的有机磷(OP)杀虫剂是很常见的。儿童的解毒机制要到出生后几年才发育完善。儿童中神经发育障碍病例的增加,以及他们对 OP 神经毒性的易感性增加,不能仅用遗传因素来解释,而可能与基因-环境相互作用有关。对氧磷酶 1(PON1)是一种可以解毒 OP 的酶,但它对某些 OP 的水解催化效率受到 Q192R 多态性的调节。动物研究提供了重要信息,表明 PON1 在保护妊娠期和产后免受 OP 毒性方面的作用。PON1Q192 等位基因在水解某些 OP 方面的效率低于 PON1R192 等位基因。母体 PON1 状态(PON1 活性水平,最重要的测量指标,以及功能性 Q192R 表型)调节接触 OP 氯氧磷对胎儿大脑基因表达和暴露生物标志物的不利影响。流行病学研究表明,来自母体 PON1 状态较低的母亲在怀孕期间接触 OP 的儿童,出生时头围较小,儿童期认知功能出现不良影响。婴儿和儿童容易受到 OP 毒性的影响。OP 对神经发育的有害影响可能导致下一代出现永久性认知问题,并易患神经退行性疾病。需要使用质谱法监测 OP 加合物生物标志物的改进方法,这将对生命早期生物监测非常有帮助,而测量 PON1 状态作为易感性的生物标志物将有助于识别对 OP 高度敏感的母亲和儿童。使用加合物组学而不是酶活性测定来监测 OP 暴露已被证明具有几个优势,包括使用干血斑,这将方便监测新生儿和儿童。