Petersen Richard C
Biomaterials, SDB 539, 1919 7th Avenue South, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Biomedical Research Technologies, 3830 Avenida Del Presidente, M/S 36, San Clemente, CA, 92674, USA.
AIMS Biophys. 2017;4(2):240-283. doi: 10.3934/biophy.2017.2.240. Epub 2017 Apr 6.
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.
在病理化学领域有一项突破，涉及到分子结构的增加，这种结构会干扰氧气通过细胞膜的扩散。自由基可通过链式增长聚合反应，将不饱和低粘度脂肪酸油交联成更粘稠的液体甚至固体。线粒体在间歇性缺氧时会释放自由基，这可能会增加膜分子的有序性，从而降低流动性和氧气扩散，有可能朝着病理疾病形成持续的恶性循环。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态。氧原子和氮原子中的成对电子要求氧键旋转、氮键反转，以寻找极性纳米环境并避开非极性纳米环境，从而在非极性膜和极性生物流体界面产生波动的不稳定性。随后的机械分子运动提供自由能，以通过分子和氧气的膜运输增加其扩散进入细胞，还包括细胞膜信号传导/识别/防御以及蛋白质运动以进行酶混合。在其他化学过程中，钙与主要位于质膜外表面的膜磷酸盐结合，以影响膜兴奋性的激发阈值，并更好地阻止水渗透。由于钙是一种优良的金属导体，而膜磷酸盐头部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进行安全传导，从而具有更广泛的耗散潜力。关于医疗状况，自由基已知会引发病理变化，尤其是在与年龄相关的疾病以及衰老过程中。由于癌细胞膜呈现出极端的多态性，这在研究中已得到广泛关注，因此开发了易于观察的自由基模型。在治疗方面，使用据称是抗氧化剂可清除自由基的维生素营养补充剂，在临床试验中并未证明有价值，这可能是由于早期基于不准确比色法测试的抗氧化剂测量存在误差。然而，更新的共价键收缩测试现在能够为自由基抑制剂对苯二酚和其他分子用于药物治疗提供准确测量。
