Dopamine Quinone Research Articles

Oxidative Stress and Dopaminergic Metabolism: A Major PD Pathogenic Mechanism and Basis of Potential Antioxidant Therapies

Reactive oxygen species (ROS)-induced oxidative stress triggers the vicious cycle leading to the degeneration of dopaminergic neurons in the nigra pars compacta. ROS produced during the metabolism of dopamine is immediately neutralized by the endogenous antioxidant defense system (EADS) under physiological conditions. Aging decreases the vigilance of EADS and makes the dopaminergic neurons more vulnerable to oxidative stress. As a result, ROS left over by EADS oxidize the dopamine-derived catechols and produces a number of reactive dopamine quinones, which are precursors to endogenous neurotoxins. In addition, ROS causes lipid peroxidation, uncoupling of the electron transport chain, and DNA damage, which lead to mitochondrial dysfunction, lysosomal dysfunction, and synaptic dysfunction. The mutations in genes such as DNAJC6, SYNJ1, SH3GL2, LRRK2, PRKN, and VPS35 caused by ROS have been associated with synaptic dysfunction and the pathogenesis of Parkinson’s disease (PD). The available drugs that are used against PD can only delay the progression of the disease, but they produce various side effects. Through their antioxidant activity, flavonoids can substantiate the EADS of dopaminergic neurons and disrupt the vicious cycle incepted by oxidative stress. In this review, we show how the oxidative metabolism of dopamine generates ROS and dopamine-quinones, which then exert unrestrained OS, causing mutations in several genes involved in the proper functioning of mitochondrion, synapse, and lysosome. Besides, we also present some examples of approved drugs used for the treatment of PD, therapies in the clinical trial phase, and an update on the flavonoids that have been tested to boost the EADS of dopaminergic neurons.

MnO2 nanosheets based catechol oxidase mimics for robust electrochemical sensor: Synthesis, mechanism and its application for ultrasensitive and selective detection of dopamine

Nanozymes have favorable activity and good stability, which are potential alternatives to natural enzymes and widely applied in biosensing. However, nanozymes based electrochemical sensors are fewer, because many nanozymes are not easy to form efficient electrocatalytic interface and experience interference from the possible oxidizable species. Herein, ultrathin MnO2 nanosheets (MnO2 NSs) were synthesized by reduction of KMnO4 in acidic environment by chemical precipitation method. The MnO2 NSs show excellent catechol oxidase mimicking activity. The steady-state kinetics of MnO2 NSs shows a higher Vmax of 3.441 µM s−1. Additionally, the catalytic mechanism is that in the presence of oxygen, catechol or its analogues are oxidized to quinone or quinoids, while oxygen is reduced to H2O. Afterwards, the possible mechanism of dopamine (DA) at MnO2 NSs-modified electrode is investigated. DA is first catalytically oxidized to dopamine quinone (DQ) by MnO2 NSs based catechol oxidase, which further undergoes irreversible electrochemical reduction to DA involving two protons and two electrons transfer during the process. On the basis of this, a selective and ultrasensitive amperometric detection of DA at 0.0 V (vs. SCE) was explored, which have two linear parts, 0.01–20 μM and 20–100 μM DA with the LOD of 4.1 nM (S/N = 3). Most importantly, the presence of oxidizable species including ascorbic acid, uric acid and cysteine may coexist with DA in biological systems do not exhibit any appreciable interference. The as-proposed method was applicable to detect DA in human serum samples with good satisfactory accuracy and recovery. This research casts prospect to apply nanozymes for electrochemical sensor with excellent analytical performance.

SERS-Based Microneedle Biosensor for In Situ and Sensitive Detection of Tyrosinase.

Tyrosinase (TYR) emerges as a key enzyme that exerts a regulatory influence on the synthesis of melanin, thereby assuming the role of a critical biomarker for the detection of melanoma. Detecting the authentic concentration of TYR in the skin remains a primary challenge. Distinguished from ex vivo detection methods, this study introduces a novel sensor platform that integrates a microneedle (MN) biosensor with surface-enhanced Raman spectroscopy (SERS) technology for the in situ detection of TYR in human skin. The platform utilized dopamine (DA)-functionalized gold nanoparticles (Au NPs) as the capturing substrate and 4-mercaptophenylboronic acid (4-MPBA)-modified silver nanoparticles (Ag NPs) acting as the SERS probe. Here, the Au NPs were functionalized with mercaptosuccinic acid (MSA) for DA capture. In the presence of TYR, DA immobilized on the MN is preferentially oxidized to dopamine quinone (DQ), a process that results in a decreased density of SERS probes on the platform. TYR concentration was detected through variations in the signal intensity emitted by the phenylboronic acid. The detection system was able to evaluate TYR concentrations within a linear range of 0.05 U/mL to 200 U/mL and showed robust anti-interference capabilities. The proposed platform, integrating MN-based in situ sensing, SERS technology, and TYR responsiveness, holds significant importance for diagnosing cutaneous melanoma.

Robust Zeolitic Tetrazole Framework for Electrocatalytic Dopamine Detection with High Selectivity.

A novel zeolitic tetrazolate framework (ZTF-8) has been synthesized by solvent-free heat-assisted (70 °C) mechanochemical grinding of zinc acetate and 5-methyl tetrazole in the presence of NaOH powder. The structure of ZTF-8 adopts the zeolitic sodalite (SOD) topology with uncoordinated N-heteroatom sites and resembles the structure of the well-known zeolitic imidazole framework ZIF-8. ZTF-8 is exceptionally stable in 0.1 M aqueous acid and base solutions for 60 days at 25 °C. The unique structure with uncoordinated N-heteroatom active sites and exceptional stability of ZTF-8 facilitated the electrocatalytic oxidation of dopamine to dopamine quinone at neutral pH. Without any postsynthetic modification, ZTF-8 is directly used for the facile electrochemical detection of dopamine over a wide range of concentrations (5-550 μM) with a high sensitivity (2410.8 μA mM-1 cm-2). It also demonstrated promising selectivity over other interferents of similar oxidation potential, such as ascorbic acid and uric acid. The DFT study revealed that the ZTF-8 framework has a higher binding energy (-145.07 kJ/mol) and stronger interaction with dopamine than its isostructural ZIF-8 structure (-130.42 kJ/mol).

LuMA-Functionalized Thermosensitive Hydrogel: A Versatile and Robust Dopamine-Triggered Platform for Diverse Biomolecules Sensing.

It is of great significance for the analysis of multiple biomarkers because a single biomarker is difficult to accurately achieve early diagnosis, disease course monitoring, and prognosis evaluation. Herein, a luminescence thermosensitive hydrogel was synthesized by radical polymerization using a methacrylic acid derivative monomer of luminol (LuMA) as luminescent, N-isopropylacrylamide (NIPAM) as thermosensitive monomer, and acrydite-oligonucleotides [dopamine (DA) aptamer, DNA C1, and DNA C2] as recognition elements. The combined DA based on the affinity interaction between the DA and the aptamer on the hydrogel polymer chain was electrochemically oxidized to dopamine quinone during the electrochemiluminescence (ECL) scanning, which effectively quenched the ECL signal of LuMA due to the resonance energy transfer (RET). In addition, the thermosensitive hydrogel showed swelling-collapse characteristics when the temperature was below and above the volume phase transition temperature. Undergoing the collapse process initiated by the temperature, the RET efficiency was further enhanced due to the shortened distance between the energy donor and acceptor, showing a 1.4 times signal amplification and achieving sensitive detection of DA with a limit of detection (LOD) of 1.7 × 10-10 M. For a proof of concept application, coupled with the target-induced release of DA from the DNA-magnetic beads bioconjugations based on duplex-specific nuclease (DSN)-assisted target recycling amplification strategy and DNAzyme cleavage reaction, this ECL-RET approach was successfully used to evaluate multiple targets including miRNA-141 and MUC1 with the LOD of 2.5 aM and 1.6 fg/mL, respectively. The excellent performances of the versatile and robust ECL-RET hydrogel in multiple target sensing showed potential applications in clinical diagnosis and disease therapeutic assay.

Electrochemical Sensor Based on Co-Doped FePS3 Nanosheets for Ultra-Sensitive Detection of Dopamine in Human Serum

Electrochemical dopamine (DA) sensors become important for the early diagnosis of psychiatric disorders like schizophrenia and Parkinson’s disease due to their fast response, simplicity, and portability. However, traditional electrode modification materials such as noble metals and metal oxides have shortcomings such as high cost, low conductivity, or limited catalytic performance. Two-dimensional sulfide materials contribute to the smooth electrode reaction because of their ultra-high specific superficial area and favorable electrocatalysis properties, however, their low carrier mobility and poor electroconductibility limit the detection signal. In this paper, Co-doped FePS3 nanosheets were employed for DA detection for the first time. Fe0.9Co0.1PS3 nanosheets exhibited a detection limit of 120 nM, a linear range 0.25–100 μM and 120–500 μM, and possessed high recovery and reproducible stability when applied to human serum samples. Furthermore, according to the in situ XPS characterization, S atoms located on the outmost layer of Fe0.9Co0.1PS3 nanosheets could be combined with the phenolic hydroxyl oxygen of DA, which makes electrode reaction from DA to dopamine quinone easier. Co-doping can further enhance the above effect, and increase the carrier mobility of FePS3 nanosheets. This work demonstrated electrochemical sensors based on metal phosphorus trisulfide materials have tremendous potential for future application in mental disorder diagnosis.

Cathodic electrochemiluminescence based on resonance energy transfer between sulfur quantum dots and dopamine quinone for the detection of dopamine

Herein, an ultrasensitive electrochemiluminescence (ECL) sensor was established for the determination of dopamine using sulfur quantum dots (SQDs) as the luminophore. The detection mechanism highlights how dopamine can be oxidized into dopamine quinone (DQ) and quenches the ECL signal of SQDs. Under the optimized experimental conditions, the ECL signal of SQDs was used for the detection of dopamine in the linear range of 1 × 10−10 to 1 × 10−3 M with a detection limit of 2.5 × 10−11 M (S/N = 3). The proposed method has excellent specificity, a low detection limit, and high sensitivity when applied in the analysis of real samples and is applicable in the development of novel ECL luminophores as well as the improvement of human health.

Transformation of L-DOPA and Dopamine on the Surface of Gold Nanoparticles: An NMR and Computational Study.

Gold nanoparticles (AuNPs) have found applications in biomedicine as diagnostic tools, but extensive research efforts have been also directed toward their development as more efficient drug delivery agents. The high specific surface area of AuNPs may provide dense loading of molecules like catechols (L-DOPA and dopamine) on nanosurfaces, enabling functionalization strategies for advancing conventional therapy and diagnostic approaches of neurodegenerative diseases. Despite numerous well-described procedures in the literature for preparation of different AuNPs, possible transformation and structural changes of surface functionalization agents have not been considered thoroughly. As a case in point, the catechols L-DOPA and dopamine were selected because of their susceptibility to oxidation, cyclization, and polymerization. To assess the fate of coating and functionalization agents during the preparation of AuNPs or interaction at the nano-bio interface, a combination of spectroscopy, light scattering, and microscopy techniques was used while structural information and reaction mechanism were obtained by NMR in combination with computational tools. The results revealed that the final form of catechol on the AuNP nanosurface depends on the molar ratio of Au used for AuNP preparation. A large molar excess of L-DOPA or dopamine is needed to prepare AuNPs funtionalized with fully reduced catechols. In the case of molar excess of Au, the oxidation of catechols to dopamine quinone and dopaquinone was promoted, and dopaquinone underwent intramolecular cyclization in which additional oxidation products, leukodopachrome, dopachrome, or its tautomer, were formed because of the larger intrinsic acidity of the more nucleophilic amino group in dopaquinone. MD simulations showed that, of the oxidation products, dopachrome had the highest affinity for binding to the AuNPs surface. The results highlight how a more versatile methodological approach, combining experimental and in silico techniques, allows more reliable characterization of binding events at the surface of AuNPs for possible applications in biomedicine.

Multifunctional coating of cotton fabric via the assembly of amino-quinone networks with polyamine biomacromolecules and dopamine quinone

Functional textiles with antibacterial properties and UV protection are essential for human health. However, the process of functional modification of textiles is usually done with the help of chemical cross-linking agents to improve the bonding fastness of functional finishing agents on textiles. The use of chemical cross-linking agents is not eco-friendly enough and is prone to chemical waste. In this study, some highly reactive polyamine biomolecules were combined with dopamine quinone, a super adhesive bionic material, to spontaneously construct amino-quinone networks (AQNs) coatings on the surface of cotton fabrics without the addition of chemical crosslinkers. The amino/quinone compounds (A/Q) self-crosslinking reaction is achieved by Michael addition and Schiff base reaction between the quinone group in dopamine quinone and the amino group in chitosan (CTS), chitooligosaccharide (COS) or ԑ-polylysine (ԑ-PL). The combination of polyamines and dopamine quinone during the cotton finishing process imparts antibacterial and UV protection to cotton fabric. The results showed that the AQNs coating modified fabrics had superb UV protection and antibacterial rates of over 96% against both E. coli and S. aureus. In addition, the AQNs coating modified fabrics had good resistance to washing and mechanical abrasion. This study proposes that self-assembled amino-quinone network multifunctional coatings of dopamine quinone and polyamine biomolecules are of guiding significance for the development of environmentally friendly bio-based materials.

Dopamine decreases LPS-induced expression of proinflammatory cytokines in microglial cells through the formation of dopamine quinone in the mouse striatum.

Dopamine decreases LPS-induced expression of proinflammatory cytokines in microglial cells through the formation of dopamine quinone in the mouse striatum.

Dopamine inhibits the expression of proinflammatory cytokines of microglial cells through the formation of dopamine quinone in the mouse striatum

We previously reported that dopamine (DA) attenuated lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines through the formation of DA quinone (DAQ) in murine microglial cell line BV-2 and primary murine microglial cells. To reveal whether DA inhibits the expression of proinflammatory cytokines of microglial cells through the formation of DAQ in the central nervous system (CNS), in this study, we examined the effect of DAQ on LPS-induced mRNA expression of proinflammatory cytokines in C57BL/6 mouse brain under two experimental conditions: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration and l-dopa/carbidopa administration. Acute MPTP administration reduced the number of tyrosine hydroxylase-positive cells in the substantia nigra, and decreased the level of quinoprotein, an indicator of DAQ formation, in the striatum. Real-time RT-PCR analysis revealed that intraperitoneal administration of LPS increased the mRNA levels of proinflammatory cytokines, including tumor-necrosis factor-α and interleukin-1β, in the striatum. These increases were enhanced in MPTP-treated mice. On the other hand, l-dopa/carbidopa administration increased the level of quinoprotein, attenuated the LPS-induced mRNA expression of proinflammatory cytokines, and reduced the LPS-induced increase in the number of microglial cells in the striatum. These results suggest that DA attenuate the expression of proinflammatory cytokines in microglia through the formation of DAQ in the CNS.

Effect of Chronic Methylphenidate Treatment in a Female Experimental Model of Parkinsonism.

Methylphenidate (MPH) is the most commonly prescribed drug for the treatment of ADHD in males and females. However, a majority of previous studies investigated the effect of MPH in only males, and little is known regarding consequences of female exposure to MPH. This is unfortunate because the few studies that have been conducted indicate that females have a greater sensitivity to MPH. Previous research in male mice has shown that chronic exposure to MPH causes dopaminergic neurons within the nigrostriatal pathway to be more sensitive to the Parkinsonian toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). However, estrogen has been shown to protect dopaminergic neurons from MPTP neurotoxicity. Therefore, in this study, we test the hypothesis that chronic MPH exposure in female mice will render dopaminergic neurons in the nigrostriatal pathway more sensitive to MPTP, and that estrogen may play a protective role. Interestingly, proestrus females exhibited greater sensitivity to MPTP, with significantly reduced dopaminergic neurons in the SN and significant increases in DA quinone production. Chronic MPH exposure contributed to GSH depletion, but surprisingly, it did not increase dopamine quinone levels or dopaminergic cell loss. There were no significant differences in anestrus animals, with the exception of a depletion in GSH seen when animals received chronic high-dose (10mg/kg) MPH followed by MPTP. Thus, estrogen may actually sensitize neurons to MPTP in this model, and chronic MPH may contribute to GSH depletion within the striatum. This study provides insight into how chronic psychostimulant use may affect males and females differently.

Molecular Pharmacology of NRH:Quinone Oxidoreductase 2: A Detoxifying Enzyme Acting as an Undercover Toxifying Enzyme.

N-ribosyldihydronicotinamide:quinone oxidoreductase 2 (NQO2/QR2, Enzyme Commission number 1.10.99.2) is a cytosolic enzyme, abundant in the liver and variably expressed in mammalian tissues. Cloned 30 years ago, it was characterized as a flavoenzyme catalyzing the reduction of quinones and pseudoquinones. To do so, it uses exclusively N-alkyl nicotinamide derivatives, without being able to recognize NADH, the reference hydrure donor compound, in contrast to its next of a kind, NAD(P)H:quinone oxidoreductase 1 (NQO1). For a long time both enzymes have been considered as key detoxifying enzymes in quinone metabolism, but more recent findings point to a more toxifying function of NQO2, particularly with respect to ortho-quinones. In fact, during the reduction of substrates, NQO2 generates fairly unstable intermediates that reoxidize immediately back to the original quinone, creating a futile cycle, the byproducts of which are deleterious reactive oxygen species. Beside this peculiarity, it is a target for numerous drugs and natural compounds such as melatonin, chloroquine, imiquimod, resveratrol, piceatannol, quercetin, and other flavonoids. Most of these enzyme-ligand interactions have been documented by numerous crystallographic studies, and now NQO2 is one of the best represented proteins in the structural biology database. Despite evidence for a causative role in several important diseases, the functional role of NQO2 remains poorly explored. In the present review, we aimed at detailing the main characteristics of NQO2 from a molecular pharmacology perspective. By drawing a clear border between facts and speculations, we hope to stimulate the future research toward a better understanding of this intriguing drug target. SIGNIFICANCE STATEMENT: Evidence is reviewed on the prevalent toxifying function of N-ribosyldihydronicotinamide:quinone oxidoreductase 2 while catalyzing the reduction of ortho-quinones such as dopamine quinone. The product of this reaction is unstable and generates a futile but harmful cycle (substrate/product/substrate) associated with reactive oxygen species generation.

Alpha-Synuclein Dopaminylation Presented in Plasma of Both Healthy Subjects and Parkinson's Disease Patients.

Alpha-synuclein (α-syn) dopaminylation can lead to the death of dopaminergic neurons in the brain and is a risk factor of Parkinson's disease (PD). This study aims to examine whether such a posttranslational modification (PTM) is presented in human blood plasma. In vitro reaction simulation between α-syn and dopamine (DA) is conducted to study the biochemical mechanism. Then α-syn from human blood plasma samples is detected by using immunoprecipitation-mass spectrometry (IP-MS). Lastly the levels of endogenous α-syn and α-syn dopaminylation in 88 blood plasma samples from patients with PD, major depressive disorder (MDD), and healthy control (HC) are compared. DA modifies α-syn with the addition of dopamine-quinone (DAQ) into lysine sites of α-syn in vitro and the addition of DAQ and 3,4-dihydroxyphenylacetaldehyde (DOPAL) in plasma samples. The unmodified α-syn between the PD and HC groups showed similar levels. The levels of two peptides, one with lysine 34 (34 K) DAQ modification and the other with lysine 23 (23 K) ubiquitination, are significantly higher in PD and MDD compared with HC. Thus, α-syn dopaminylation is measurable and might be used to indicatethe presence and progression of neurological disorders.

Nature inspired poly (dopamine quinone -vanadyl) as new modifier for voltammetric determination of uric acid.

Thepreparation of a novel polymer (poly(dopamine quinone-vanadyl) (polyDQV)) bearing dopaminequinone and VOIV redox groupsis described. PolyDQV was characterized using field emission scanning electron microscopy (FESEM), energy dispersive x-ray spectroscopy, x-ray photoelectron spectroscopy (XPS), Fourier transform infra-red (FTIR) spectroscopy, UV-Vis spectroscopy as well as electrochemical methods such as differential pulse voltammetry, cyclic voltammetry, and electrochemical impedance spectroscopy (EIS). The electrocatalytic activity of polyDQV was studied toward electrooxidation of uric acid using differential pulse voltammetry as well as cyclic voltammetry. PolyDQV presents interesting electrocatalytic activity toward UA oxidation in phosphate buffer solution (0.1M, pH2) to a well-defined oxidation peak at 0.65V (vs. Ag/AgCl). The polyDQV-modified carbon paste electrode (CPE/polyDQV) presents a precise linear signal-concentration relationship in the ranges of 0.3-5μM and 5 to 200μM with a detection limit (S/N = 3) of 0.02μM. The %RSD values for ten replicate measurements of 0.5 and 50μM UA were 1.8 and 3%, respectively, indicating good repeatability of analytical signals. Appropriate recovery values (in the range 96 to 103%) and good selectivity for UA over common coexisting species (such as ascorbic acid and dopamine) exhibit that CPE/polyDQV is a promising novel platform for sensing UA in human blood serum and urine samples. Graphical abstract.

NMR Spectroelectrochemistry in Studies of Dopamine Oxidation

In this paper, the electrochemical oxidation of dopamine was studied by using gold nanoparticles modified nano-polyaniline film as the catalyst. Electrochemistry and nuclear magnetic resonance spectroscopy (EC–NMR) was used to investigate electro-catalytic mechanism and evaluate the electro-catalytic capacity. The influence of varied pH values and voltages in the electrocatalytic process was studied. The oxidation mechanism of dopamine can be proposed: (1) at pH 1 and 600 mV, the main oxidation product is dopamine quinone (DQ). Only a small amount of DQ occurs cyclization reaction to form quinone aminochrome (AC); (2) at pH 1 and 800 mV, the oxidation products are DQ and 5,6-dihydroxyindole (DHI). (3) With the pH value increases, the oxidation of dopamine steps over DQ and AC, and directly produces DHI. DHI is aggregated to form melanin sediment. Our results indicate that the gold nanoparticles modified electrode displays high catalytic performance toward dopamine electrochemical oxidation.

A sensitive resonance Rayleigh scattering sensor for dopamine in urine using upconversion nanoparticles

AbstractA highly sensitive resonance light scattering method for detecting dopamine in urine was developed by using a novel probe based on lanthanide‐doped upconversion nanoparticles (UCNPs) linked to dopamine–quinone (DQ) by hydrogen bonding and electrostatic interactions. Adding dopamine to a solution containing UCNPs decreases their size and the intensity of their resonance light scattering signals. Based on the decrease, dopamine can be determined in Tris–HCl buffer and in urine samples spiked with analyte concentrations over the range 0–300 μM with a limit of detection of 1.62 μM. As‐prepared UD can thus provide an effective platform for biosensor development, drug discovery, and rapid diagnosis of Parkinson's and Alzheimer's disease, among other medical conditions.

Dopamine attenuates lipopolysaccharide-induced expression of proinflammatory cytokines by inhibiting the nuclear translocation of NF-κB p65 through the formation of dopamine quinone in microglia.

Many reports have indicated that dopamine has immunomodulatory effects on peripheral immune cells. The purpose of this study was to reveal the immunomodulatory effect of dopamine on the expression of proinflammatory cytokines in microglial cells, which are the immune cells of the central nervous system. In murine microglial cell line BV-2 cells, pretreatment with dopamine for 24 h attenuated the lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines such as tumor-necrosis factor-α, interleukin-1β, and interleukin-6. Neither (5R)-8-chloro-3-methyl-5-phenyl-1,2,4,5-tetrahydro-3-benzazepin-7-ol; hydrochloride (SCH-23390) nor sulpiride, which are dopamine D1-like and D2-like receptor antagonists, respectively, affected the attenuation of LPS-induced expression of cytokines by dopamine. In addition, pretreatment with neither (−)-(6aR,12bR)-4,6,6a,7,8,12b-Hexahydro-7-methylindolo[4,3-a]phenanthridin (CY208-243) nor bromocriptine, dopamine D1-like and D2-like receptor agonists, respectively, was effective in doing so. However, N-acetylcysteine (NAC), which inhibits dopamine oxidation to dopamine quinone, did inhibit this attenuated expression. Dopamine increased the level of quinoproteins, and this increase was inhibited by NAC. Western blot and immunocytochemical analyses revealed that dopamine inhibited LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB) p65. Dopamine also attenuated the expression of cytokines and the nuclear translocation of NF-κB p65 induced by LPS in mouse microglial cells in primary culture. These results suggest that dopamine attenuated LPS-induced expression of cytokines by inhibiting the nuclear translocation of NF-κB p65 through the formation of dopamine quinone in microglial cells.

Colorimetric analysis of the early oxidation of dopamine by hypochlorous acid as preliminary screening tool for chemical determinants of neuronal oxidative stress

The hypochlorous acid produced by the innate immune system during inflammation characteristic of several neurodegenerative disorders is responsible for the generation of chlorinated byproducts of dopamine in neurons where this neurotransmitter reaches the highest concentration. Therefore, this physiological acid could play a key role in neuronal oxidative stress associated to aberrant dopamine-quinones (DQ) production. Here we report a model study simulating simplified conditions of HOCl reaction with dopamine (DA) in neurons, showing for the first time that DA is immediately converted by HOCl to the yellow colored DQ molecule. The DQ originated from dopamine oxidation results directly proportional to the total amount of the oxidant with excellent reproducibility. Furthermore, following the several evidences of the interplay between cytosolic dopamine and calcium in neurodegenerative disorders, we have verified that the presence of calcium cation influences the dopamine oxidation pathway likely due to the metal chelation by semiquinone formed in the early stage of dopamine oxidation. This experimental approach, based on the isolation of the highly reactive DQ molecule, could be useful for prelaminar investigation of the (putative) determinants of dopamine-poisoning derivatives formation.

A high sensitive and selective fluorescent probe for dopamine detection based on water soluble AgInS2 quantum dots

Herein, a water soluble AgInS2 quantum dots (AIS QDs) with high sensitive and selective for dopamine (DA) were prepared through a clean and facile reflux method with the mercapto propionic acid (MPA) and polyethyleneimine (PEI) used as the co-modifiers. The fluorescence quench of as-fabricated AIS QDs displayed an excellent selectivity and sensitivity to the DA and they showed a good linear relationship with the low detection limit (2.84 nm) in the range of 0.5–300 μmol/L. The mechanism of fluorescence quench may attributed to the photoinduced electrons migrated from AIS QDs to dopamine quinone, which originated from the oxidization of DA by ambient O2. Our work shows a promising prospect of designing and preparing AIS QDs used as the fluorescence sensors for DA detection.