Kinetics analysis of H2S oxidation by human sulfide quinone oxidoreductase

Nitric Oxide ◽  
2014 ◽  
Vol 42 ◽  
pp. 151
Author(s):  
Pramod Kumar Yadav ◽  
Ruma Banerjee
Keyword(s):  
Kinetics Analysis ◽  
Quinone Oxidoreductase ◽  
H2s Oxidation

scholarly journals H2S oxidation by nanodisc-embedded human sulfide quinone oxidoreductase

2017 ◽  
Vol 292 (28) ◽  
pp. 11641-11649 ◽  
Author(s):  
Aaron P. Landry ◽  
David P. Ballou ◽  
Ruma Banerjee
Keyword(s):  
Quinone Oxidoreductase ◽  
H2s Oxidation

scholarly journals A redox cycle with complex II prioritizes sulfide quinone oxidoreductase dependent H2S oxidation

2021 ◽  
pp. 101435
Author(s):  
Roshan Kumar ◽  
Aaron P. Landry ◽  
Arkajit Guha ◽  
Victor Vitvitsky ◽  
Ho Joon Lee ◽  
...  
Keyword(s):  
Redox Cycle ◽  
Quinone Oxidoreductase ◽  
Complex Ii ◽  
H2s Oxidation

Processing Nigerian pyrolusite ore, Part I: Characterization and dissolution kinetics analysis

CIM Journal ◽  
2016 ◽  
Vol 7 (1) ◽  
pp. 43-51 ◽  
Author(s):  
A. A. Baba ◽  
L. Ibrahim ◽  
R. B. Bale ◽  
A. G. F. Alabi ◽  
F. A. Adekola ◽  
...  
Keyword(s):  
Dissolution Kinetics ◽  
Kinetics Analysis

Inhibition of NADPH: Quinone Oxidoreductase Activity of Camel Lens ζ-Crystallin by Colchicine

2015 ◽  
Vol 10 (2) ◽  
pp. 137-142
Author(s):  
Ibrahim A. Alharbi ◽  
Majid Khan ◽  
Nayyar Rabbani ◽  
Abdulrahman M. Al-Senaidy ◽  
Mohammad A. Ismael ◽  
...  
Keyword(s):  
Quinone Oxidoreductase ◽  
Oxidoreductase Activity

Kinetics Analysis of Reaction between Molybdenum and Nitrogen Trifluoride

2021 ◽  
Vol 49 (4) ◽  
pp. e21039-e21045
Author(s):  
Yong-Sheng NIU ◽  
Li-Xin SUN ◽  
Cong-Wei HU ◽  
Jin-Hao ZHOU ◽  
Qiang DOU ◽  
...  
Keyword(s):  
Kinetics Analysis ◽  
Nitrogen Trifluoride

scholarly journals Study of deposition parameters and growth kinetics of ZnO deposited by aerosol assisted chemical vapor deposition

RSC Advances ◽  
2021 ◽  
Vol 11 (30) ◽  
pp. 18493-18499
Author(s):  
Sergio Sánchez-Martín ◽  
S. M. Olaizola ◽  
E. Castaño ◽  
E. Urionabarrenetxea ◽  
G. G. Mandayo ◽  
...  
Keyword(s):  
Chemical Vapor Deposition ◽  
Growth Kinetics ◽  
Vapor Deposition ◽  
Chemical Vapor ◽  
Kinetics Analysis ◽  
Deposition Parameters ◽  
Kinetics Of

Impact of deposition parameters, microstructure and growth kinetics analysis of ZnO grown by Aerosol-assisted Chemical Vapor Deposition (AACVD).

scholarly journals Mitigation of Aflatoxin B1 Hepatoxicity by Dietary Hedyotis diffusa Is Associated with Activation of NRF2/ARE Signaling in Chicks

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 878
Author(s):  
Ling Zhao ◽  
Jiang Deng ◽  
Zi-Jian Xu ◽  
Wan-Po Zhang ◽  
Mahmoud Mohamed Khalil ◽  
...  
Keyword(s):  
Aflatoxin B1 ◽  
Body Weight Gain ◽  
Control Diet ◽  
Protein Carbonyl ◽  
Heme Oxygenase 1 ◽  
High Dose ◽  
Feed Conversion ◽  
Quinone Oxidoreductase ◽  
Vacuolar Degeneration ◽  
Hedyotis Diffusa

The objective of this study was to explore the mechanism of Hedyotis diffusa (HD) in mediating the detoxification of aflatoxin B1 (AFB1)-induced hepatic injury in chicks. A total of 144 one-day-old male broilers (Cobb 500) were randomly assigned to four treatment groups (n = 6 cages/diet, 6 chicks/cage). After three days of acclimation, the broilers were fed either a control diet (Control), Control plus 0.5 mg/kg of AFB1, or Control plus 0.5 mg/kg AFB1 with 500 or 1000 mg/kg HD for two weeks. Both serum and liver were collected at the end of the feeding trial for biochemistry, histology, and NF-E2-related nuclear factor 2 (NRF2)/antioxidant response element (ARE) signaling analysis. Compared with Control, the AFB1 treatment caused liver injury and decreased (p < 0.05) body weight gain, feed intake, feed conversion ratio, and serum albumin and total protein by 6.2–20.7%. AFB1 also induced swelling, necrosis, and severe vacuolar degeneration in chicks’ livers. Notably, HD supplementation at 500 and 1000 mg/kg mitigated (p < 0.05) the alterations induced by AFB1. HD supplementation alleviated (p < 0.05) AFB1-induced impairment in hepatic glutathione peroxidase activity, protein carbonyl, and exo-AFB1-8,9-epoxide (AFBO)–DNA concentrations by 57.7–100% and increased (p < 0.05) the activities of superoxide dismutase and catalase by 23.1–40.9% more than those of AFB1 treatment alone. Furthermore, HD supplementation at the two doses upregulated (p < 0.05) NRF2, NAD(P)H: quinone oxidoreductase-1, heme oxygenase-1, glutathione cysteine ligase catalytic subunit, and glutathione-S transferase A2 and A3 in livers relative to the AFB1 group by 0.99–3.4-fold. Overall, dietary supplementation of HD at a high dose displayed better protection effects against aflatoxicosis. In conclusion, a dietary HD supplementation at 500 and 1000 mg/kg protected broilers from AFB1-induced hepatotoxicity, potentially due to the activation of NRF2/ARE signaling in the chicks.

scholarly journals Kinetic Constraints in the Specific Interaction between Phosphorylated Ubiquitin and Proteasomal Shuttle Factors

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1008
Author(s):  
Ling-Yun Qin ◽  
Zhou Gong ◽  
Kan Liu ◽  
Xu Dong ◽  
Chun Tang
Keyword(s):  
Exchange Rate ◽  
Self Assembly ◽  
Solution Structure ◽  
Specific Interaction ◽  
Dissociation Rate ◽  
Fine Tuning ◽  
Binding Mechanism ◽  
Kinetics Analysis ◽  
Kinetic Constraint ◽  
Thermodynamic Basis

Ubiquitin (Ub) specifically interacts with the Ub-associating domain (UBA) in a proteasomal shuttle factor, while the latter is involved in either proteasomal targeting or self-assembly coacervation. PINK1 phosphorylates Ub at S65 and makes Ub alternate between C-terminally relaxed (pUbRL) and retracted conformations (pUbRT). Using NMR spectroscopy, we show that pUbRL but not pUbRT preferentially interacts with the UBA from two proteasomal shuttle factors Ubqln2 and Rad23A. Yet discriminatorily, Ubqln2-UBA binds to pUb more tightly than Rad23A does and selectively enriches pUbRL upon complex formation. Further, we determine the solution structure of the complex between Ubqln2-UBA and pUbRL and uncover the thermodynamic basis for the stronger interaction. NMR kinetics analysis at different timescales further suggests an indued-fit binding mechanism for pUb-UBA interaction. Notably, at a relatively low saturation level, the dissociation rate of the UBA-pUbRL complex is comparable with the exchange rate between pUbRL and pUbRT. Thus, a kinetic constraint would dictate the interaction between Ub and UBA, thus fine-tuning the functional state of the proteasomal shuttle factors.

scholarly journals Apigenin and Luteolin Regulate Autophagy by Targeting NRH-Quinone Oxidoreductase 2 in Liver Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 776
Author(s):  
Elzbieta Janda ◽  
Concetta Martino ◽  
Concetta Riillo ◽  
Maddalena Parafati ◽  
Antonella Lascala ◽  
...  
Keyword(s):  
Potential Role ◽  
Autophagic Flux ◽  
Ampk Activation ◽  
Amp Kinase ◽  
Quinone Oxidoreductase ◽  
Ampk Phosphorylation ◽  
Autophagy Induction ◽  
Ampk Activity ◽  
Dietary Flavonoids

Dietary flavonoids stimulate autophagy and prevent liver dysfunction, but the upstream signaling pathways triggered by these compounds are not well understood. Certain polyphenols bind directly to NRH-quinone oxidoreductase 2 (NQO2) and inhibit its activity. NQO2 is highly expressed in the liver, where it participates in quinone metabolism, but recent evidence indicates that it may also play a role in the regulation of oxidative stress and autophagy. Here, we addressed a potential role of NQO2 in autophagy induction by flavonoids. The pro-autophagic activity of seven flavonoid aglycons correlated perfectly with their ability to inhibit NQO2 activity, and flavones such as apigenin and luteolin showed the strongest activity in all assays. The silencing of NQO2 strongly reduced flavone-induced autophagic flux, although it increased basal LC3-II levels in HepG2 cells. Both flavones induced AMP kinase (AMPK) activation, while its reduction by AMPK beta (PRKAB1) silencing inhibited flavone-induced autophagy. Interestingly, the depletion of NQO2 levels by siRNA increased the basal AMPK phosphorylation but abrogated its further increase by apigenin. Thus, NQO2 contributes to the negative regulation of AMPK activity and autophagy, while its targeting by flavones releases pro-autophagic signals. These findings imply that NQO2 works as a flavone receptor mediating autophagy and may contribute to other hepatic effects of flavonoids.

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