Free-radicals and advanced chemistries involved in cell membrane organization influence oxygen diffusion and pathology treatment.

IF 1.1 Q4 BIOPHYSICS
AIMS Biophysics Pub Date : 2017-01-01 Epub Date: 2017-04-06 DOI:10.3934/biophy.2017.2.240
Richard C Petersen
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引用次数: 31

Abstract

A breakthrough has been discovered in pathology chemistry related to increasing molecular structure that can interfere with oxygen diffusion through cell membranes. Free radicals can crosslink unsaturated low-viscosity fatty acid oils by chain-growth polymerization into more viscous liquids and even solids. Free radicals are released by mitochondria in response to intermittent hypoxia that can increase membrane molecular organization to reduce fluidity and oxygen diffusion in a possible continuing vicious cycle toward pathological disease. Alternate computational chemistry demonstrates molecular bond dynamics in free energy for cell membrane physiologic movements. Paired electrons in oxygen and nitrogen atoms require that oxygen bonds rotate and nitrogen bonds invert to seek polar nano-environments and hide from nonpolar nano-environments thus creating fluctuating instability at a nonpolar membrane and polar biologic fluid interface. Subsequent mechanomolecular movements provide free energy to increase diffusion by membrane transport of molecules and oxygen into the cell, cell-membrane signaling/recognition/defense in addition to protein movements for enzyme mixing. In other chemistry calcium bonds to membrane phosphates primarily on the outer plasma cell membrane surface to influence the membrane firing threshold for excitability and better seal out water permeation. Because calcium is an excellent metal conductor and membrane phosphate headgroups form a semiconductor at the biologic fluid interface, excess electrons released by mitochondria may have more broad dissipation potential by safe conduction through calcium atomic-sized circuits on the outer membrane surface. Regarding medical conditions, free radicals are known to produce pathology especially in age-related disease in addition to aging. Because cancer cell membranes develop extreme polymorphism that has been extensively followed in research, accentuated easily-visualized free-radical models are developed. In terms of treatment, use of vitamin nutrient supplements purported to be antioxidants that remove free radicals has not proved worthwhile in clinical trials presumably due to errors with early antioxidant measurements based on inaccurate colorimetry tests. However, newer covalent-bond shrinkage tests now provide accurate measurements for free-radical inhibitor hydroquinone and other molecules toward drug therapy.

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自由基和参与细胞膜组织的高级化学物质影响氧扩散和病理治疗。
在病理化学中发现了一个突破,与增加分子结构有关,可以干扰氧气通过细胞膜的扩散。自由基可以通过链式聚合将不饱和低粘度脂肪酸油交联成粘度更高的液体甚至固体。线粒体在间歇性缺氧时释放自由基,增加细胞膜分子组织,减少流动性和氧气扩散,可能形成持续的恶性循环,最终导致病理性疾病。交替计算化学展示了细胞膜生理运动中自由能的分子键动力学。氧原子和氮原子中的配对电子需要氧键旋转和氮键反转来寻找极性纳米环境并躲避非极性纳米环境,从而在非极性膜和极性生物流体界面上产生波动不稳定性。随后的机械分子运动提供自由能量,通过分子和氧气的膜运输增加扩散,细胞膜信号/识别/防御以及酶混合的蛋白质运动。在其他化学反应中,钙主要在外质细胞膜表面与膜磷酸盐结合,从而影响膜兴奋性的放电阈值,并更好地阻止水渗透。由于钙是一种优良的金属导体,膜磷酸盐头基团在生物流体界面形成半导体,线粒体释放的多余电子可能通过外膜表面钙原子大小的电路安全传导,具有更广泛的耗散电位。在医疗条件方面,除了衰老之外,自由基还会产生病理,特别是与年龄有关的疾病。由于癌细胞膜的极端多态性在研究中得到了广泛的关注,因此开发了易于可视化的自由基模型。在治疗方面,使用维生素营养补充剂据称是抗氧化剂,可以清除自由基,在临床试验中没有被证明是值得的,这可能是由于早期抗氧化剂测量基于不准确的比色法测试的错误。然而,新的共价键收缩测试现在为自由基抑制剂对苯二酚和其他分子的药物治疗提供了精确的测量。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
AIMS Biophysics
AIMS Biophysics BIOPHYSICS-
CiteScore
2.40
自引率
20.00%
发文量
16
审稿时长
8 weeks
期刊介绍: AIMS Biophysics is an international Open Access journal devoted to publishing peer-reviewed, high quality, original papers in the field of biophysics. We publish the following article types: original research articles, reviews, editorials, letters, and conference reports. AIMS Biophysics welcomes, but not limited to, the papers from the following topics: · Structural biology · Biophysical technology · Bioenergetics · Membrane biophysics · Cellular Biophysics · Electrophysiology · Neuro-Biophysics · Biomechanics · Systems biology
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