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Gln192Arg polymorphism in paraoxonase 1 gene is associated with Alzheimer disease in a Chinese Han ethnic population

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Chinese Medical Journal 2006年第14期119卷 1204-1209页

作者： HE Xiao-ming ZHANG Zhen-xin ZHANG Jun-wu ZHOU Yong-tao TANG Mou-ni WU Cheng-bin HONG Zhen Department of Neurology Peking Union Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100730 China National Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences of Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100730 China Institute of Mental Health West China Hospital Sichuan University Chengdu 610065 China Department of Neurology First Affiliated Hospital Xi＇an Jiaotong University Xi＇an 710049 China Institute of Neurology Huashan Hospital Fudan University Shanghai 200040 China Department of Neurology Xiangfan Hospital Affiliated to Tongji Medical College Huazhong University of Science and Technolgy Xiangfan 441021 China

Background Oxidative stress such as low-density lipoprotein （LDL） oxidation is thought to be an important mechanism in Alzheimer＇s disease （AD）. paraoxonase 1 （PON1）, an enzyme located on high-density lipoprotein, can prevent LDL from oxidation to some extent. It is also a potent cholinesterase inhibitor and an arylesterase, combating organophosphate poisoning and metabolization of environmental neurotoxins which might be responsible for neurodegeneration with *** evaluated the association of Gln192Arg polymorphism in the PON1 gene with AD in a Chinese Han ethnic population. Methods Patients and age-matched controls were recruited from outpatient clinics and a population-based epidemiological survey, respectively. Gln192Arg polymorphism in the PON1 gene was detected by allele-specific PCR technique in 521 patients with AD and 578 healthy controls. Results The presence of at least one of PON1 R alleles （Q/R or R/R） was lower in AD patients than in the controls （82.7% vs 87.4%; χ^2 = 4.68, P = 0.03）. PON1 gene R allele frequency was lower in AD patients than in the controls （60.7% vs 64.7%; χ^2=3.85, P = 0.05）. One-way ANOVA showed that PON1 genotype had no effect on the age of onset for developing AD. Logistic regression analysis demonstrated the age and sex-adjusted odds ratio （OR） for the risk of AD in PON1 of PON1 R allele carriers was 0.71 （P = 0.044, 95%CI, 0.51 - 0.99）.Conclusion Our results indicate that Gln192Arg polymorphism in the PON1 gene is associated with AD, and PON1 R allele might be a protective factor for AD in a Chinese Han ethnic population.

关键词： Alzheimer disease paraoxonase 1 gene single nucleotide polymorphism

Pros and Cons in Therapeutic Evaluation of paraoxonase 1 in Nerve Agent Toxicity

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Journal of Life Sciences 2013年第9期7卷 935-940页

作者： Manojkumar Valiyaveettil Yonas Alamneh Bhupendra P. Doctor Alfred M. Sciuto Madhusoodana P.Nambiar Blast-Induced Neurotrauma Branch Center for Military Psychiatry and Neuroscience Walter Reed Army Institute of ResearchSilver Spring MD 20910 USA Analytical Toxicology Division US Army Medical Research Institute of Chemical Defense Aberdeen Proving Ground MD21010 USA

PON 1 （paraoxonase 1） has been proposed as an efficient catalytic bioscavenger to combat against OP （organophosphate） and CWNA （chemical warfare nerve agent） toxicity. Unlike stoichiometric bioscavengers such as butyrylcholinesterase, catalytic bioscavengers are cost effective with the advantage of eliminating all the OPs/CWNAs at low doses. Analysis of catalytic bioscavenger efficacy of PONI showed promising results by various group of researchers. Still, there are large numbers of grey areas which are not addressed so far. One of the major areas of interest is the pharmacokinetic analysis of infused PON 1 in multiple animal models. It is shown that previous studies in mice significantly increased half-life of PONI, while recent studies in guinea pigs from our group showed reduced half-life of PON1. Similar results were reported by other research groups in guinea pigs and non-human primates. The short half-life of exogenously administered PON1 in multiple animal models may be due to poor association of PON1 with its endogenous carrier, high density lipoprotein or lower doses of PON 1 or a reflection of species difference. These observations warrant the significance of thorough pharmacokinetic analysis of infused PON 1 and the development of alternative approaches for successful utility of PON 1 as an efficient medical countermeasure against OP/CWNA toxicity.

关键词： paraoxonase 1 catalytic bioscavenger chemical warfare nerve agents pharmacokinetics protective efficacy

Plasma paraoxonase 1,Oxidized Low Density Lipoprotein,and Lipid Peroxidation Levels in Gout Patients

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Plasma Paraoxonase 1,Oxidized Low Density Lipoprotein,and Li...

Novel neuroprotective and hepatoprorective effects of citric acid in acute malathion intoxication

中华医学会第九次全国检验医学学术会议暨中国医院协会临床...

作者： Xing-liang Jiang~1,Min Li~2,Jing-guo Zhou~2,Qi-bin Yang~2,Li-jun Du~2,Juan Du~1 1 Department of Medical Laboratory Science, Affiliated Hospital of North Sichuan Medical College,Nanchong 2 Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College,Nanchong

Objectives Increasing evidence suggests that patients with gout have a high incidence of atherosclerotic coronary heart *** serum paraoxonase(PON) activity is thought to be a risk factor for the development of *** connection between PON1 activity and oxidative stress measures and atherosclerosis in gout has not been *** present study was designed to

关键词： Gout paraoxonase 1 Oxidized low density lipoprotein Lipid peroxidation

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Asian Pacific Journal of Tropical Medicine 2016年第12期9卷 1157-1169页

作者： Omar M.E.Abdel-Salam Eman R.Youness Nadia A.Mohammed Noha N.Yassen Yasser A.Khadrawy Safinaz Ebrahim El-Toukhy Amany A.Sleem Department of Toxicology and Narcotics National Research Centre Medical Biochemistry National Research Centre Pathology National Research Centre Physiology National Research Centre Pharmacology National Research Centre

Objective: To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure. Methods: Rats were received intraperitoneal(i.p.) injection of malathion 150 mg/kg along with citric acid(200 or 400 mg/kg, orally), atropine(1 mg/kg, i.p.) or citric acid 200 mg/kg+atropine 1 mg/kg and euthanized 4 h later. Results: Malathion resulted in increased lipid peroxidation(malondialdehyde) and nitric oxide concentrations accompanied with a decrease in brain reduced glutathione, glutathione peroxidase(GPx) activity, total antioxidant capacity(TAC) and glucose concentrations. paraoxonase-1, acetylcholinesterase(ACh E) and butyrylcholinesterase activities decreased in brain as well. Liver aspartate aminotransferase and alanine aminotransferase activities were raised. The Comet assay showed increased DNA damage of peripheral blood lymphocytes. Histological damage and increased expression of inducible nitric oxide synthase(i NOS) were observed in brain and liver. Citric acid resulted in decreased brain lipid peroxidation and nitric oxide. Meanwhile, glutathione, GPx activity, TAC capacity and brain glucose level increased. Brain ACh E increased but PON1 and butyrylcholinesterase activities decreased by citric acid. Liver enzymes, the percentage of damaged blood lymphocytes, histopathological alterations and i NOS expression in brain and liver was decreased by citric acid. Meanwhile, rats treated with atropine showed decreased brain MDA, nitrite but increased GPx activity, TAC, ACh E and glucose. The drug also decreased DNA damage of peripheral blood lymphocytes, histopathological alterations and i NOS expression in brain and liver. Conclusions: The study demonstrates a beneficial effect for citric acid upon brain oxidative stress, neuronal injury, liver and DNA damage due to acute malathion exposure.

关键词： Citric acid Malathion Oxidative stress paraoxonase 1 Cholinesterase Comet assay

Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development

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World Journal of Methodology 2021年第4期11卷 144-159页

作者： Renee J Dufault Mesay M Wolle H M Skip Kingston Steven G Gilbert Joseph A Murray Food Ingredient and Health Research Institute NaalehuHI 96772United States College of Graduate Health Studies A.T.Still UniversityKirksvilleMO 63501United States Department of Chemistry and Biochemistry Duquesne UniversityPittsburghPA 15282United States Institute of Neurotoxicology and Neurological Disorders SeattleWA 98105United States Division of Gastroenterology and Hepatology Mayo ClinicRochesterMN 55905United States

Pre-natal and post-natal chemical exposures and co-exposures from a variety of sources including contaminated air,water,soil,and food are common and associated with poorer birth and child health *** diet is a contributing factor in the development of child behavioral *** behavior and learning can be adversely impacted when gene expression is altered by dietary transcription factors such as zinc insufficiency or deficiency or by exposure to toxic substances permitted in our food supply such as mercury,lead,or organophosphate pesticide *** with autism spectrum disorder and attention deficit hyperactivity disorders exhibit decreased or impaired PON1 gene activity which is needed by the body to metabolize and excrete neurotoxic organophosphate *** this current review we present an updated macroepigenetic model that explains how dietary inorganic mercury and lead exposures from unhealthy diet may lead to elevated blood mercury and/or lead levels and the development of symptoms associated with the autism and attention deficithyperactivity ***1 gene activity may be suppressed by inadequate dietary calcium,selenium,and fatty acid intake or exposures to lead or *** model may assist clinicians in diagnosing and treating the symptoms associated with these childhood neurodevelopmental *** for future research are provided based on the updated model and review of recently published literature.

关键词： Autism paraoxonase 1 Selenium Inorganic mercury Lead Attention deficit hyperactivity disorder

Effect of Astragalin on Paraoxon-induced Vascular Endothelium Dysfunction

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Plant Diseases and Pests 2011年第2期2卷 73-76页

作者：李鹏尹雅玲潘国聘赵繁荣王倩倩新乡医学院医学院河南新乡453003 新乡医学院基础医学院河南新乡453003

[ Objective] The paper was to explore the effect of astragalin on paraoxon-indueed vascular endothelium dysfunction and analyze the potential mecha- nism. [Method]The isolated rat thoracic aorta rings were exposed to medium contained paraoxon （3.63 μmol/L）, and astragalin （10 μmol/L） was used to inhib- it the damage effect. Rat thoracic aorta rings were suspended in organ chambers to assess vas orelaxation activity in vitro by acetyleholine （ACh）-induced endotheli- um dependent relaxation reaction （EDRR） and sodium nitroprusside （SNP）-induced endothdium-independent relaxation reaction. [Result]The exposure to parao- xon （3.63 μmol/L） resulted in an inhibition of the EDRR, markedly reduced the level of nitric oxide （NO）, the activity of paraoxonasel （PON1） and superoxide dismutase （SOD）, and significantly increased the level of malondialdehyde （MDA） in isolated rat thoracic aorta. However, the presence of astragalin （10 μmol/L） markedly attenuated the vascular endothelium dysfunction induced by paraoxon via increasing level of NO, activity of PON1 and SOD, as well as reducing level of MDA. In addition, treatment of astragalin （ 10 μmol/L） showed a similar effect to hydrogen peroxide （ 1.0 μmol/L）, a kind of antioxidant, on paraoxon- induced vascular endothelium dysfunction. [ Conclusion] Astragalin could protect the vascular endothelium against the paraoxon-induced dysfunction in isolated rat thoracic aorta, and＇the beneficial effects of astragalin might be concerned with the antioxidation of astragalin due to inhibiting the decreased activity of PONI.

关键词： Astragalin Paraoxon Oxidative stress paraoxonase 1

Genotype and haplotype association of PONlwith susceptibility to coronary artery diseaseand clinical outcomes in dual antiplatelet-treated Han Chinese patients

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Genotype and haplotype association of PONlwith susceptibilit...