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人类退行性疾病的物理化学基础

Physiochemical basis of human degenerative disease.

作者信息

Zeliger Harold I, Lipinski Boguslaw

机构信息

Zeliger Research and Consulting, Cape Elizabeth, Maine, USA.

Harvard Medical School, Joslin Diabetes Center, Boston, Massachusetts, USA.

出版信息

Interdiscip Toxicol. 2015 Mar;8(1):15-21. doi: 10.1515/intox-2015-0003.

DOI:10.1515/intox-2015-0003
PMID:27486355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4961921/
Abstract

The onset of human degenerative diseases in humans, including type 2 diabetes, cardiovascular disease, neurological disorders, neurodevelopmental disease and neurodegenerative disease has been shown to be related to exposures to persistent organic pollutants, including polychlorinated biphenyls, chlorinated pesticides, polybrominated diphenyl ethers and others, as well as to polynuclear aromatic hydrocarbons, phthalates, bisphenol-A and other aromatic lipophilic species. The onset of these diseases has also been related to exposures to transition metal ions. A physiochemical mechanism for the onset of degenerative environmental disease dependent upon exposure to a combination of lipophilic aromatic hydrocarbons and transition metal ions is proposed here. The findings reported here also, for the first time, explain why aromatic hydrocarbons exhibit greater toxicity than aliphatic hydrocarbons of equal carbon numbers.

摘要

人类退行性疾病的发生,包括2型糖尿病、心血管疾病、神经紊乱、神经发育疾病和神经退行性疾病,已被证明与接触持久性有机污染物有关,这些污染物包括多氯联苯、氯化农药、多溴二苯醚等,以及与多核芳烃、邻苯二甲酸盐、双酚A和其他芳香亲脂性物质有关。这些疾病的发生也与接触过渡金属离子有关。本文提出了一种依赖于接触亲脂性芳烃和过渡金属离子组合的退行性环境疾病发病的物理化学机制。本文报道的研究结果还首次解释了为什么芳烃比同等碳原子数的脂肪烃具有更大的毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6a1/4961921/a519eec34e24/ITX-8-015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6a1/4961921/a519eec34e24/ITX-8-015-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6a1/4961921/a519eec34e24/ITX-8-015-g001.jpg

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本文引用的文献

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Interdiscip Toxicol. 2014 Sep;7(3):117-22. doi: 10.2478/intox-2014-0016. Epub 2014 Dec 30.
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Cytoglobin ligand binding regulated by changing haem-co-ordination in response to intramolecular disulfide bond formation and lipid interaction.细胞红蛋白配体结合通过响应分子内二硫键形成和脂质相互作用改变血红素配位来调节。
Biochem J. 2015 Jan 1;465(1):127-37. doi: 10.1042/BJ20140827.
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Correlations among heavy metals in blood and urine and their relations to depressive symptoms in Parkinson's disease patients.
帕金森病患者血液和尿液中重金属之间的相关性及其与抑郁症状的关系。
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Polyaromatic hydrocarbons do not disturb liquid-liquid phase coexistence, but increase the fluidity of model membranes.多环芳烃不会干扰液-液相共存,但会增加模型膜的流动性。
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Genetic factors and manganese-induced neurotoxicity.遗传因素与锰诱导的神经毒性。
Front Genet. 2014 Aug 4;5:265. doi: 10.3389/fgene.2014.00265. eCollection 2014.
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Cancer wars: significance of protein unfolding in cancer and its inhibition with natural amphiphilic substances.癌症之战:蛋白质解折叠在癌症中的意义及其被天然两亲性物质抑制的情况
Front Oncol. 2014 Jul 11;4:183. doi: 10.3389/fonc.2014.00183. eCollection 2014.
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Association of Parkinson's disease with altered serum levels of lead and transition metals among South Indian subjects.印度南部人群中帕金森病与血清铅及过渡金属水平改变的关联。
Indian J Biochem Biophys. 2014 Apr;51(2):121-6.
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Interactions of metals and Apolipoprotein E in Alzheimer's disease.金属与载脂蛋白 E 在阿尔茨海默病中的相互作用。
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Metal-PAH mixtures in the aquatic environment: a review of co-toxic mechanisms leading to more-than-additive outcomes.金属多环芳烃混合物在水生态环境中的协同毒性机制研究进展:致非加和性效应的探讨。
Aquat Toxicol. 2014 Sep;154:253-69. doi: 10.1016/j.aquatox.2014.05.026. Epub 2014 Jun 2.