1.
A combined experimental and computational study on the oxidative degradation of bromophenols by Fe(VI) and the formation of self-coupling products.
Dar, AA, Chen, J, Shad, A, Pan, X, Yao, J, Bin-Jumah, M, Allam, AA, Huo, Z, Zhu, F, Wang, Z
Environmental pollution (Barking, Essex : 1987). 2020;:113678
Abstract
In this study, the degradation of eight bromophenols (BPs), including monobromophenols (2-BP, 3-BP, and 4-BP), dibromophenols (2,4-DBP, 2,6-DBP, and 3,5-DBP), a tribromophenol (2,4,6-TBP) and a pentabromophenol (PBP), by a Fe(VI) reaction process at a pH of 8.0 was systematically studied. It was concluded that their degradation rates increased with increasing Fe(VI) concentrations in solution. The removal of 2,4,6-TBP, 2-BP, and 2,6-DBP was faster than that of the other five BPs, which could be attributed to the position of the substituting Br atom. Moreover, the direct oxidation and coupling reactions greatly influenced the reactivity of the bromophenols with Fe(VI). The electron paramagnetic resonance (EPR) analysis confirmed the presence of hydroxyl radicals in present system. The oxidation reaction products of PBP and 2-BP were recognized by an electrospray time-of-flight mass spectrometer; hydroxylation, hydroxyl substitution, the cleavage of the C-C bond, direct oxidation and polymerization via an end linking mechanism were noticeably found in the reaction process, resulting in the formation of polymerization products and causing hydroxylation to occur. Theoretical calculations further determined the possible oxidation sites of 2-BP and PBP. This study may provide comprehensive and important information on the remediation of BPs by Fe(VI).
2.
Catalytic Mechanism for 2,3-Dihydroxybiphenyl Ring Cleavage by Nonheme Extradiol Dioxygenases BphC: Insights from QM/MM Analysis.
Wang, J, Chen, J, Tang, X, Li, Y, Zhang, R, Zhu, L, Sun, Y, Zhang, Q, Wang, W
The journal of physical chemistry. B. 2019;(10):2244-2253
Abstract
An extradiol-cleaving catecholic dioxygenase, 2,3-dihydroxybiphenyl dioxygenase, plays important roles in the catabolism of biphenyl/polychlorinated biphenyl aromatic contaminants in the environment. To better elucidate the biodegradable pathway, a theoretical investigation of the ring-opening degradation of 2,3-dihydroxybiphenyl (DHBP) was performed with the aid of quantum mechanical/molecular mechanical calculations. A quintet state of the DHBP-iron-dioxygen group adducts was found to be the reactive state with a substrate radical-FeII-superoxo (DHBP•↑-FeII-O2•-↓) character. The HOO• species was the reactive oxygen species responsible for the subsequent attack of DHBP. Among the whole reaction energy profile, the first step in proton-coupled electron transfer was determined to be the rate-determining step with a potential energy barrier of 17.2 kcal/mol, which is close to the experimental value (14.7 kcal/mol). Importantly, the residue His194 shows distinct roles in the catalytic cycle, where it acts as an acid-base catalyst to deprotonate the hydroxyl group of DHBP at an early stage, then stabilizes the negative charge on the dioxygen group, and, at the final stage, promotes the semialdehyde product formation as a proton donor.
3.
Overexpressed Hsp70 alleviated formaldehyde-induced apoptosis partly via PI3K/Akt signaling pathway in human bronchial epithelial cells.
Liu, L, Huang, Y, Feng, X, Chen, J, Duan, Y
Environmental toxicology. 2019;(4):495-504
Abstract
Formaldehyde (FA) is a ubiquitous environmental pollutant, which can induce apoptosis in lung cell and is related to the pathogenesis of asthma, pneumonia, and chronic obstructive pulmonary disease. Heat shock protein 70 (Hsp70) is an ATP-dependent molecular chaperone and exhibits an anti-apoptosis ability in a variety of cells. Previous studies reported that the expression of Hsp70 was induced when organisms were exposed to FA. Whether Hsp70 plays a role in the FA-induced apoptosis and the involved cell signaling pathway remain largely unknown. In this study, human bronchial epithelial cells with overexpressed Hsp70 and the control were exposed to different concentrations of FA (0, 40, 80, and 160 μmol/L) for 24 hours. Apoptosis and the expression levels of PI3K, Akt, p-Akt, MEK, p-MEK, and GLI2 were detected by Annexin-APC/7AAD double-labeled flow cytometry and western blot. The results showed that overexpression of Hsp70 decreased the apoptosis induced by FA and alleviated the decline of PI3k and p-Akt significantly. Inhibitor (LY 294002, a specific inhibitor of PI3K-Akt) test result indicated that PI3K-Akt signaling pathway was involved in the inhibition of FA-induced apoptosis by Hsp70 overexpression and also active in the maintenance of GLI2 level. However, it also suggested that other signaling pathways activated by overexpressed Hsp70 participated in this process, which was needed to be elucidated in further research.