• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

质膜辅酶Q:自闭症中作用的证据

Plasma membrane coenzyme Q: evidence for a role in autism.

作者信息

Crane Frederick L, Löw Hans, Sun Iris, Navas Placido, Gvozdjáková Anna

机构信息

Department of Biological Sciences, Purdue University, West Lafayette, IN, USA.

Department of Molecular Medicine, Karolinska Institute, Stockholm, Sweden.

出版信息

Biologics. 2014 May 29;8:199-205. doi: 10.2147/BTT.S53375. eCollection 2014.

DOI:10.2147/BTT.S53375
PMID:24920882
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4043426/
Abstract

BACKGROUND

The Voltage Dependent Anion Channel (VDAC) is involved in control of autism. Treatments, including coenzyme Q, have had some success on autism control.

DATA SOURCES

Correlation of porin redox activity and expression of autism is based on extensive literature, especially studies of antibodies, identification of cytosolic nicotinamide adenine dinucleotide reduced (NADH) dehydrogenase activity in the VDAC, and evidence for extreme sensitivity of the dehydrogenase to a mercurial. Evidence for a coenzyme Q requirement came from extraction and analog inhibition of NADH ferricyanide reductase in the erythrocyte plasma membrane, done in 1994, and reinterpreted when it was identified in VDAC in 2004. The effects of ubiquinol (the QH2 - reduced form of coenzyme Q) in children with autism were studied.

RESULTS

A new role for coenzyme Q in the porin channels has implications on autism. Ubiquinol, the more active form of coenzyme Q, produces favorable response in children with autism. Agents which affected electron transport in porin show parallel effects in autism.

CONCLUSION

We propose a hypothesis that autism is controlled by a coenzyme Q-dependent redox system in the porin channels; this conclusion is based on the effects of agents that positively or negatively affect electron transport and the symptoms of autism. The full understanding of the mechanism of their control needs to be established.

摘要

背景

电压依赖性阴离子通道(VDAC)参与自闭症的调控。包括辅酶Q在内的治疗方法在自闭症控制方面已取得一定成效。

数据来源

孔蛋白氧化还原活性与自闭症表达之间的相关性基于大量文献,特别是关于抗体的研究、VDAC中胞质烟酰胺腺嘌呤二核苷酸还原型(NADH)脱氢酶活性的鉴定,以及该脱氢酶对汞剂极度敏感的证据。辅酶Q需求的证据来自1994年对红细胞质膜中NADH铁氰化物还原酶的提取和类似物抑制研究,并在2004年在VDAC中鉴定出来后进行了重新解读。对泛醇(辅酶Q的还原形式QH2)在自闭症儿童中的作用进行了研究。

结果

辅酶Q在孔蛋白通道中的新作用对自闭症有影响。泛醇,即辅酶Q更具活性的形式,在自闭症儿童中产生了良好的反应。影响孔蛋白中电子传递的物质在自闭症中表现出类似的作用。

结论

我们提出一个假说,即自闭症由孔蛋白通道中依赖辅酶Q的氧化还原系统控制;这一结论基于对电子传递有正向或负向影响的物质的作用以及自闭症的症状。其控制机制的全面理解有待确立。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/046d/4043426/e9d8dde8345c/btt-8-199Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/046d/4043426/e9d8dde8345c/btt-8-199Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/046d/4043426/e9d8dde8345c/btt-8-199Fig1.jpg

相似文献

1
Plasma membrane coenzyme Q: evidence for a role in autism.质膜辅酶Q:自闭症中作用的证据
Biologics. 2014 May 29;8:199-205. doi: 10.2147/BTT.S53375. eCollection 2014.
2
Evidence for a relation between plasma membrane coenzyme Q and autism.
Front Biosci (Elite Ed). 2013 Jun 1;5(3):1011-6. doi: 10.2741/e680.
3
Requirement for coenzyme Q in plasma membrane electron transport.质膜电子传递中辅酶Q的需求
Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11126-30. doi: 10.1073/pnas.89.23.11126.
4
Genetic evidence for coenzyme Q requirement in plasma membrane electron transport.质膜电子传递中辅酶Q需求的遗传证据。
J Bioenerg Biomembr. 1998 Oct;30(5):465-75. doi: 10.1023/a:1020542230308.
5
Putting together a plasma membrane NADH oxidase: a tale of three laboratories.组装质膜 NADH 氧化酶:三个实验室的故事。
Int J Biochem Cell Biol. 2012 Nov;44(11):1834-8. doi: 10.1016/j.biocel.2012.06.032. Epub 2012 Jun 29.
6
Evidence for coenzyme Q function in transplasma membrane electron transport.辅酶Q在跨质膜电子传递中功能的证据。
Biochem Biophys Res Commun. 1990 Nov 15;172(3):979-84. doi: 10.1016/0006-291x(90)91542-z.
7
Coenzyme Q reductase from liver plasma membrane: purification and role in trans-plasma-membrane electron transport.来自肝细胞膜的辅酶Q还原酶:纯化及其在跨细胞膜电子传递中的作用
Proc Natl Acad Sci U S A. 1995 May 23;92(11):4887-91. doi: 10.1073/pnas.92.11.4887.
8
VDAC1 is a transplasma membrane NADH-ferricyanide reductase.电压依赖性阴离子通道1是一种跨质膜的NADH-铁氰化物还原酶。
J Biol Chem. 2004 Feb 6;279(6):4811-9. doi: 10.1074/jbc.M311020200. Epub 2003 Oct 22.
9
New findings concerning vertebrate porin II--on the relevance of glycine motifs of type-1 VDAC.关于脊椎动物 porin II 的新发现——关于 1 型 VDAC 甘氨酸基序的相关性。
Mol Genet Metab. 2013 Apr;108(4):212-24. doi: 10.1016/j.ymgme.2013.01.008. Epub 2013 Jan 26.
10
RESPIRATORY PATHWAYS IN THE MYCOPLASMA. II. PATHWAY OF ELECTRON TRANSPORT DURING OXIDATION OF REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE BY MYCOPLASMA HOMINIS.支原体中的呼吸途径。II. 人型支原体氧化还原型烟酰胺腺嘌呤二核苷酸时的电子传递途径。
J Bacteriol. 1964 Jul;88(1):122-9. doi: 10.1128/jb.88.1.122-129.1964.

引用本文的文献

1
Testing Green Tea Extract and Ammonium Salts as Stimulants of Physical Performance in a Forced Swimming Rat Experimental Model.检测绿茶提取物和铵盐对强迫游泳大鼠实验模型的身体性能的刺激作用。
Int J Mol Sci. 2024 Sep 27;25(19):10438. doi: 10.3390/ijms251910438.
2
Multikingdom and functional gut microbiota markers for autism spectrum disorder.用于自闭症谱系障碍的多菌种和功能性肠道微生物群标志物。
Nat Microbiol. 2024 Sep;9(9):2344-2355. doi: 10.1038/s41564-024-01739-1. Epub 2024 Jul 8.
3
Animal Models of Coenzyme Q Deficiency: Mechanistic and Translational Learnings.

本文引用的文献

1
Hyperbaric oxygen treatment in autism spectrum disorders.自闭症谱系障碍的高压氧治疗
Med Gas Res. 2012 Jun 15;2(1):16. doi: 10.1186/2045-9912-2-16.
2
Altered neurotrophin, neuropeptide, cytokines and nitric oxide levels in autism.自闭症患者的神经营养因子、神经肽、细胞因子和一氧化氮水平改变。
Pharmacopsychiatry. 2012 Sep;45(6):241-3. doi: 10.1055/s-0032-1301914. Epub 2012 Mar 16.
3
Prostacyclin receptor-mediated ATP release from erythrocytes requires the voltage-dependent anion channel.前列腺素 I2 受体介导电致红细胞释放三磷酸腺苷需要电压依赖性阴离子通道。
辅酶Q缺乏的动物模型:机制与转化研究
Antioxidants (Basel). 2021 Oct 26;10(11):1687. doi: 10.3390/antiox10111687.
4
An Overview of the Main Genetic, Epigenetic and Environmental Factors Involved in Autism Spectrum Disorder Focusing on Synaptic Activity.自闭症谱系障碍主要遗传、表观遗传和环境因素概述——聚焦于突触活动。
Int J Mol Sci. 2020 Nov 5;21(21):8290. doi: 10.3390/ijms21218290.
5
Neuroprotective potential of solanesol in intracerebroventricular propionic acid induced experimental model of autism: Insights from behavioral and biochemical evidence.茄尼醇对脑室内注射丙酸诱导的自闭症实验模型的神经保护潜力:行为学和生化证据的见解
Toxicol Rep. 2019 Nov 5;6:1164-1175. doi: 10.1016/j.toxrep.2019.10.019. eCollection 2019.
6
Analysis of a Sardinian Multiplex Family with Autism Spectrum Disorder Points to Post-Synaptic Density Gene Variants and Identifies as a Functionally Relevant Candidate Gene.对一个患有自闭症谱系障碍的撒丁岛多重家庭的分析指向突触后密度基因变异,并将[具体基因名称未给出]鉴定为一个功能相关的候选基因。
J Clin Med. 2019 Feb 7;8(2):212. doi: 10.3390/jcm8020212.
7
Coenzyme Q Supplementation in Aging and Disease.衰老与疾病中的辅酶Q补充
Front Physiol. 2018 Feb 5;9:44. doi: 10.3389/fphys.2018.00044. eCollection 2018.
8
Frederick Loring Crane (1925-2016): Discoverer of coenzyme Q10 and rediscoverer of plastoquinone.弗雷德里克·洛林·克兰(1925 - 2016):辅酶Q10的发现者和质体醌的重新发现者。
Photosynth Res. 2017 Mar;131(3):237-239. doi: 10.1007/s11120-016-0319-x. Epub 2016 Nov 4.
9
The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.氧化应激和亚硝化应激对棕榈酰化、膜脂筏及基于脂质的细胞信号传导的有害影响:神经免疫疾病中的新药靶点
Mol Neurobiol. 2016 Sep;53(7):4638-58. doi: 10.1007/s12035-015-9392-y. Epub 2015 Aug 27.
Am J Physiol Heart Circ Physiol. 2012 Feb 1;302(3):H553-9. doi: 10.1152/ajpheart.00998.2011. Epub 2011 Dec 9.
4
Effect of a vitamin/mineral supplement on children and adults with autism.维生素/矿物质补充剂对自闭症儿童和成人的影响。
BMC Pediatr. 2011 Dec 12;11:111. doi: 10.1186/1471-2431-11-111.
5
Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis.自闭症谱系障碍中线粒体功能障碍:系统评价和荟萃分析。
Mol Psychiatry. 2012 Mar;17(3):290-314. doi: 10.1038/mp.2010.136. Epub 2011 Jan 25.
6
Chronic low-level Pb exposure during development decreases the expression of the voltage-dependent anion channel in auditory neurons of the brainstem.在发育过程中慢性低水平 Pb 暴露会降低脑干听觉神经元中电压依赖性阴离子通道的表达。
Neurotoxicology. 2010 Dec;31(6):662-73. doi: 10.1016/j.neuro.2010.08.004. Epub 2010 Aug 24.
7
Antibodies against the voltage-dependent anion channel (VDAC) and its protective ligand hexokinase-I in children with autism.自闭症儿童体内针对电压依赖性阴离子通道(VDAC)及其保护性配体己糖激酶-I的抗体。
J Neuroimmunol. 2010 Oct 8;227(1-2):153-61. doi: 10.1016/j.jneuroim.2010.06.001. Epub 2010 Jun 23.
8
Voltage-dependent anion-selective channel (VDAC) in the plasma membrane.质膜中的电压依赖性阴离子选择性通道(VDAC)。
FEBS Lett. 2010 May 3;584(9):1793-9. doi: 10.1016/j.febslet.2010.02.049. Epub 2010 Feb 23.
9
Transplasma membrane electron transport comes in two flavors.跨膜电子传递有两种形式。
Biofactors. 2008;34(3):191-200. doi: 10.3233/BIO-2009-1072.
10
Electron Pathways through Erythrocyte Plasma Membrane in Human Physiology and Pathology: Potential Redox Biomarker?人体生理与病理状态下红细胞质膜的电子传递途径:潜在的氧化还原生物标志物?
Biomark Insights. 2007 Sep 17;2:321-9.