Laboratory of Neurogenetics, Pavlov Institute of Physiology, Russian Academy of Sciences, Saint-Petersburg, Russia.
Laboratory of Regulation of the Brain Neuronal Functions, Pavlov Institute of Physiology, Russian Academy of Sciences, Saint-Petersburg, Russia.
PLoS Comput Biol. 2018 Dec 10;14(12):e1006672. doi: 10.1371/journal.pcbi.1006672. eCollection 2018 Dec.
Kynurenines, the products of tryptophan oxidative degradation, are involved in multiple neuropathologies, such as Huntington's chorea, Parkinson's disease, senile dementia, etc. The major cause for hydroxykynurenines's neurotoxicity is the oxidative stress induced by the reactive oxygen species (ROS), the by-products of L-3-hydroxykynurenine (L-3HOK) and 3-hydroxyanthranilic acid (3HAA) oxidative self-dimerization. 2-aminophenol (2AP), a structural precursor of L-3HOK and 3HAA, undergoes the oxidative conjugation to form 2-aminophenoxazinone. There are several modes of 2AP dimerization, including both enzymatic and non-enzymatic stages. In this study, the free energies for 2AP, L-3HOK and 3HAA dimerization stages have been calculated at B3LYP/6-311G(d,p)//6-311+(O)+G(d) level, both in the gas phase and in heptane or water solution. For the intermediates, ionization potentials and electron affinities were calculated, as well as free energy and kinetics of molecular oxygen interaction with several non-enzymatically formed dimers. H-atom donating power of the intermediates increases upon the progress of the oxidation, making possible generation of hydroperoxyl radical or hydrogen peroxide from O2 at the last stages. Among the dimerization intermediates, 2-aminophenoxazinole derivatives have the lowest ionization potential and can reduce O2 to superoxide anion. The rate for O-H homolytic bond dissociation is significantly higher than that for C-H bond in non-enzymatic quinoneimine conjugate. However, the last reaction passes irreversibly, reducing O2 to hydroperoxyl radical. The inorganic ferrous iron and the heme group of Drosophila phenoxazinone synthase significantly reduce the energy cost of 2AP H-atom abstraction by O2. We have also shown experimentally that total antioxidant capacity decreases in Drosophila mutant cardinal with L-3HOK excess relative to the wild type Canton-S, and lipid peroxidation decreases in aged cardinal. Taken together, our data supports the conception of hydroxykynurenines' dual role in neurotoxicity: serving as antioxidants themselves, blocking lipid peroxidation by H-atom donation, they also can easily generate ROS upon dimerization, leading to the oxidative stress development.
犬尿氨酸是色氨酸氧化降解的产物,参与多种神经病理学,如亨廷顿舞蹈症、帕金森病、老年痴呆症等。羟基犬尿氨酸(L-3HOK)和 3-羟基邻氨基苯甲酸(3HAA)氧化自二聚化产生的活性氧(ROS)引起的氧化应激是羟基犬尿氨酸神经毒性的主要原因。2-氨基酚(2AP)是 L-3HOK 和 3HAA 的结构前体,通过氧化共轭形成 2-氨基酚恶嗪酮。2AP 二聚化有几种模式,包括酶促和非酶促阶段。在这项研究中,在气相和庚烷或水溶液中,使用 B3LYP/6-311G(d,p)//6-311+(O)+G(d)水平计算了 2AP、L-3HOK 和 3HAA 二聚化阶段的自由能。对于中间体,计算了电离势和电子亲和势,以及与几种非酶形成的二聚体相互作用的自由能和动力学。随着氧化的进行,中间体的 H 供体能力增加,使得最后阶段可以从 O2 生成过氧自由基或过氧化氢。在二聚化中间体中,2-氨基酚恶嗪醇衍生物具有最低的电离势,可以将 O2 还原为超氧阴离子。O-H 均裂键的解离速率明显高于非酶醌亚胺共轭物中的 C-H 键。然而,最后一个反应是不可逆的,将 O2 还原为过氧自由基。无机亚铁和果蝇酚嗪酮合酶的血红素基团显著降低了 O2 对 2AP H 原子的抽提的能量成本。我们还通过实验表明,与野生型 Canton-S 相比,L-3HOK 过量的果蝇突变体 cardinal 的总抗氧化能力降低,而 aged cardinal 的脂质过氧化作用降低。总的来说,我们的数据支持羟基犬尿氨酸在神经毒性中双重作用的概念:作为抗氧化剂本身,通过 H 原子供体阻断脂质过氧化,它们也可以在二聚化时容易产生 ROS,导致氧化应激的发展。