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

机译:参与细胞膜组织的自由基和高级化学影响氧扩散和病理治疗

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摘要

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.
机译:在病理化学中发现了与增加分子结构有关的突破,该分子结构增加会干扰氧通过细胞膜的扩散。自由基可以通过链增长聚合反应,将不饱和的低粘度脂肪酸油交联成更粘的液体甚至固体。线粒体响应间歇性缺氧而释放出自由基,间歇性缺氧可以增加膜分子的组织,从而降低流动性和氧的扩散,从而可能导致病理性疾病的持续恶性循环。替代计算化学方法证明了细胞膜生理运动中自由能的分子键动力学。氧和氮原子中的成对电子需要氧键旋转,氮键反转以寻找极性纳米环境,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处产生波动的不稳定性。随后的机械分子运动通过分子和氧的膜运输进入细胞,提供细胞膜信号传递/识别/防御以及用于酶混合的蛋白质运动,提供了自由能以增加扩散。在其他化学方法中,钙主要与浆细胞外膜表面的磷酸膜结合,从而影响膜激发的阈值,从而更好地阻止水渗透。由于钙是极好的金属导体,而膜磷酸盐首基在生物流体界面处形成半导体,因此,通过安全地通过钙外尺寸钙表面上的电路传导,线粒体释放的过量电子可能具有更广泛的耗散潜力。关于医学状况,已知自由基除了会衰老外还会引起病理,特别是在与年龄有关的疾病中。由于癌细胞膜发展出极端的多态性,这一点已在研究中得到广泛遵循,因此开发了强调的,易于观察的自由基模型。在治疗方面,使用维生素营养补充剂声称是可以清除自由基的抗氧化剂,在临床试验中并未证明是值得的,这可能是由于基于不准确的比色法测试而进行的早期抗氧化剂测量存在误差。但是,现在,较新的共价键收缩测试为自由基抑制剂对苯二酚和其他分子的药物治疗提供了准确的测量方法。

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