Metabolic Electron Attachment as a Primary Mechanism For Toxicity Potentials of Halocarbons
Metabolic Electron Attachment as a Primary Mechanism For Toxicity Potentials of Halocarbons
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DOI：
10.2174/1573409912666160120151627
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发表时间：
2016-01-01
影响因子：
1.7
通讯作者：
Basak, Subhash C.
中科院分区：
文献类型：
--
作者：
Balasubramanian, Krishnan;Basak, Subhash C.
我们已经在Moller-Plesset二阶扰动（MP2）和一对群集单打 + CCSD和CCSD和CCSD（T）上进行了系统的大型基础，并在一组55个Haloenation Carbons的三元校正水平Crebelli毒理数据集。我们已经在优化的几何形状上计算了许多电子特性，例如垂直电子亲和力，homo-lumo间隙，偶极矩等。我们通过结合在代谢途径中的电子附着的毒性机理，通过结合与电子中的电子捐赠中的电子捐赠，从而提供了见解。肝细胞。从酶到卤代碳的电子转移伴随着键伸长，导致自动修复，这是由阴离子和中性分子的势能表面证明的。自动修复过程会导致高度反应性的自由基的产生，从而导致组织损伤，并且长时间暴露会导致肝细胞癌，具体取决于中性光碳的自由基和垂直电子亲和力的氢气倾向。
We have carried out systematic large-basis set quantum chemical computations at Moller-Plesset second-order perturbation (MP2) and couple cluster singles + doubles CCSD and CCSD(T) with triples correction levels of theories on a set of 55 halogenated carbons in the Crebelli toxicological dataset. We have computed a number of electronic properties at optimized geometries such as vertical electron affinities, HOMO-LUMO gaps, dipole moments, etc. We have provided insights into the mechanism of toxicity through electron attachment in metabolic pathways by binding to an electron donating enzyme in hepatocytes. The electron transfer from the enzyme to the halocarbon is accompanied by bond elongation resulting in autodetachment as evidenced from potential energy surfaces of the anion and neutral molecule. The autodetachment process leads to production of highly reactive free radicals, which cause tissue damage, and prolonged exposure can result in hepatocellular carcinoma depending on the hydrogen extraction propensity of the free radical and vertical electron affinity of the neutral halocarbon.