An active neurotoxic metabolite of 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE. The compound reduces dopamine levels, inhibits the biosynthesis of catecholamines, depletes cardiac norepinephrine and inactivates tyrosine hydroxylase. These and other toxic effects lead to cessation of oxidative phosphorylation, ATP depletion, and cell death. The compound, which is related to PARAQUAT, has also been used as an herbicide.
A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A family of proteins involved in the transport of organic cations. They play an important role in the elimination of a variety of endogenous substances, xenobiotics, and their metabolites from the body.
An organic cation transporter found in kidney. It is localized to the basal lateral membrane and is likely to be involved in the renal secretion of organic cations.
Integral membrane proteins of the LIPID BILAYER of SECRETORY VESICLES that catalyze transport and storage of biogenic amine NEUROTRANSMITTERS such as ACETYLCHOLINE; SEROTONIN; MELATONIN; HISTAMINE; and CATECHOLAMINES. The transporters exchange vesicular protons for cytoplasmic neurotransmitters.
A botanical insecticide that is an inhibitor of mitochondrial electron transport.
Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses (POACEAE), and woody plants. Some plants develop HERBICIDE RESISTANCE.
A group of membrane transport proteins that transport biogenic amine derivatives of catechol across the PLASMA MEMBRANE. Catecholamine plasma membrane transporter proteins regulate neural transmission as well as catecholamine metabolism and recycling.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
A class of sodium-independent nucleoside transporters that mediate the facilitative transport of NUCLEOSIDES.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
Neurons whose primary neurotransmitter is DOPAMINE.
A family of vesicular amine transporter proteins that catalyze the transport and storage of CATECHOLAMINES and indolamines into SECRETORY VESICLES.
A drug formerly used as an antipsychotic and treatment of various movement disorders. Tetrabenazine blocks neurotransmitter uptake into adrenergic storage vesicles and has been used as a high affinity label for the vesicle transport system.
The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.
An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.
A deaminated metabolite of LEVODOPA.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
Membrane proteins whose primary function is to facilitate the transport of molecules across a biological membrane. Included in this broad category are proteins involved in active transport (BIOLOGICAL TRANSPORT, ACTIVE), facilitated transport and ION CHANNELS.
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Positively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis.
The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.
An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.

Poly(ADP-ribose) polymerase activation mediates 1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. (1/255)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that causes parkinsonism in humans and nonhuman animals, and its use has led to greater understanding of the pathogenesis of Parkinson's disease. However, its molecular targets have not been defined. We show that mice lacking the gene for poly(ADP-ribose) polymerase (PARP), which catalyzes the attachment of ADP ribose units from NAD to nuclear proteins after DNA damage, are dramatically spared from MPTP neurotoxicity. MPTP potently activates PARP exclusively in vulnerable dopamine containing neurons of the substantia nigra. MPTP elicits a novel pattern of poly(ADP-ribosyl)ation of nuclear proteins that completely depends on neuronally derived nitric oxide. Thus, NO, DNA damage, and PARP activation play a critical role in MPTP-induced parkinsonism and suggest that inhibitors of PARP may have protective benefit in the treatment of Parkinson's disease.  (+info)

Comparison of the pharmacological properties of cloned rat, human, and bovine norepinephrine transporters. (2/255)

The aims of this study were to characterize the recently cloned rat norepinephrine transporter (NET) in more detail and in particular to study possible species differences in its pharmacological properties compared with the human and bovine NETs. The study was carried out by measuring the uptake of [(3)H]norepinephrine in COS-7 cells expressing the NET after transient transfection with rat, human, or bovine NET cDNA. There were small but significant differences between the rat NET and the human or bovine NETs with respect to the affinities of sodium ions (greater for rat than for bovine) of the substrates norepinephrine, epinephrine, and 1-methyl-4-phenylpyridinium (greater for human than for rat), and of the inhibitor cocaine (greater for human and bovine than for rat), whereas the affinities of dopamine and of most inhibitors, including tricyclic antidepressants, showed no species differences. The fact that the affinities for some substrates, cocaine and sodium ions exhibited small but significant interspecies differences among the rat, human, and bovine NETs suggests that ligand recognition, the translocation process, and sodium ion dependence are influenced differentially by just a few amino acid exchanges in the primary sequences of the transporters. On the other hand, the lack of any major differences in the pharmacological properties of the rat, human, and bovine NETs in this study suggests that data obtained in previous studies on rat tissues and bovine cells can be extrapolated, in all except the most quantitative analyses, to the properties of the human NET.  (+info)

LLC-PK(1) cells stably expressing the human norepinephrine transporter: A functional model of carrier-mediated norepinephrine release in protracted myocardial ischemia. (3/255)

In myocardial ischemia, adrenergic terminals undergo ATP depletion, hypoxia, and intracellular pH reduction, causing the accumulation of axoplasmic norepinephrine (NE) and intracellular Na(+) [via the Na(+)-H(+) exchanger (NHE)]. This forces the reversal of the Na(+)- and Cl(-)-dependent NE transporter (NET), triggering massive carrier-mediated NE release and, thus, arrhythmias. We have now developed a cellular model of carrier-mediated NE release using an LLC-PK(1) cell line stably transfected with human NET cDNA (LLC-NET). LLC-NET cells transported [(3)H]NE and [(3)H]N-methyl-4-phenylpyridinium ([(3)H]MPP(+)) in an inward direction. This uptake was abolished by the NET inhibitors desipramine (100 nM) and mazindol (300 nM) and by extracellular Na(+) removal. Na(+)-gradient reversal induced an efflux of (3)H-substrate from preloaded LLC-NET cells. Desipramine and mazindol blocked this efflux. Because of its greater intracellular stability and higher sensitivity to Na(+)-gradient reversal, [(3)H]MPP(+) proved preferable to [(3)H]NE as an NET substrate; therefore, only [(3)H]MPP(+) was used for subsequent studies. The K(+)/H(+) ionophore nigericin (10 microM) evoked a large efflux of [(3)H]MPP(+). This efflux was potentiated by the Na(+),K(+)-ATPase inhibitor ouabain (100 microM), was sensitive to desipramine, and was blocked by the NHE inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA; 10 microM). In contrast, EIPA failed to inhibit the [(3)H]MPP(+) efflux elicited by the Na(+) ionophore gramicidin (10 microM). Furthermore, [(3)H]MPP(+) efflux induced by the NHE-stimulant proprionate (25 mM) was negatively modulated by imidazoline receptor activation. Our findings suggest that LLC-NET cells are a sensitive model for studying transductional processes of carrier-mediated NE release associated with myocardial ischemia.  (+info)

Ion dependence of carrier-mediated release in dopamine or norepinephrine transporter-transfected cells questions the hypothesis of facilitated exchange diffusion. (4/255)

The mechanism of release mediated by the human dopamine and norepinephrine transporter (DAT and NET, respectively) was studied by a superfusion technique in human embryonic kidney 293 cells stably transfected with the respective transporter cDNA and loaded with the metabolically inert substrate [(3)H]1-methyl-4-phenylpyridinium. Release was induced by amphetamine, dopamine, and norepinephrine or by lowering the sodium or chloride concentration in the superfusion buffer (iso-osmotic replacement by lithium and isethionate, respectively). Efflux of [(3)H]1-methyl-4-phenylpyridinium was analyzed at 30-s time resolution. In both transporters, release induced by the substrates amphetamine, dopamine, and norepinephrine followed the same time course as release induced by the removal of chloride and was faster than that caused by the removal of sodium. In the presence of low sodium (DAT: 10 mM; NET: 5 mM) none of the substrates was able to induce release from either type of cell, but adding back sodium to control conditions promptly restored the releasing action. In the presence of low chloride (DAT: 3 mM; NET: 2 mM), however, amphetamine as well as the catecholamines stimulated release from both types of cell. In contrast with the ion dependence of release observed in superfusion experiments, uptake initial rates of substrates at concentrations used in release experiments were the same or even higher at low sodium than at low chloride. The results indicate a decisive role of extracellular sodium for carrier-mediated release unrelated to the sodium-dependent uptake of the releasing substrate, and suggest a release mechanism different from simple exchange diffusion considering only the amines as substrates.  (+info)

1-Methyl-4-phenyl-2,3-dihydropyridinium is transformed by ubiquinone to the selective nigrostriatal toxin 1-methyl-4-phenylpyridinium. (5/255)

We have studied the interaction of coenzyme Q with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolites, 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP(+)) and 1-methyl-4-phenylpyridinium (MPP(+)), the real neurotoxin to cause Parkinson's disease. Incubation of MPTP or MPDP(+) with rat brain synaptosomes induced complete reduction of endogenous ubiquinone-9 and ubiquinone-10 to corresponding ubiquinols. The reduction occurred in a time- and MPTP/MPDP(+) concentration-dependent manner. The reduction of ubiquinone induced by MPDP(+) went much faster than that by MPTP. MPTP did not reduce liposome-trapped ubiquinone-10, but MPDP(+) did. The real toxin MPP(+) did not reduce ubiquinone in either of the systems. The reduction by MPTP but not MPDP(+) was completely prevented by pargyline, a type B monoamine oxidase (MAO-B) inhibitor, in the synaptosomes. The results indicate that involvement of MAO-B is critical for the reduction of ubiquinone by MPTP but that MPDP(+) is a reductant of ubiquinone per se. It is suggested that ubiquinone could be an electron acceptor from MPDP(+) and promote the conversion from MPDP(+) to MPP(+) in vivo, thus accelerating the neurotoxicity of MPTP.  (+info)

The D-loop structure of human mtDNA is destabilized directly by 1-methyl-4-phenylpyridinium ion (MPP+), a parkinsonism-causing toxin. (6/255)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine has been reported to cause parkinsonism via its neurotoxic form, 1-methyl-4-phenylpyridinium ion (MPP+), which inhibits complex I of the mitochondrial respiratory chain. Its parkinsonism-causing mechanisms attract a great deal of interest as a model of the disease. Recently, we reported that MPP+ strongly decreases the amount of mtDNA independent of the inhibition of complex I. Maintenance of a proper amount of mtDNA is essential for the normal function of mitochondria as exemplified in many mitochondrial diseases. The most characteristic feature in vertebral mtDNA replication is that H-strand synthesis proceeds displacing the parental H-strand as a long single strand. It forms the D-loop, a triplex replication intermediate composed of the parental L-strand, nascent H-strand and displaced H-strand. Here we show that MPP+ does not inhibit DNA synthesis by DNA polymerase gamma, but rather releases the nascent H-strands from mtDNA both in organello and in vitro. This indicates that MPP+ directly destabilizes the D-loop structure, thereby inhibiting replication. This study raises a new mechanism, i.e. destabilization of replication intermediates, for depletion of mtDNA.  (+info)

Kinetic and selectivity differences between rodent, rabbit, and human organic cation transporters (OCT1). (7/255)

Organic cation transporters play an important role in the absorption, distribution, and elimination of clinical agents, toxic substances, and endogenous compounds. In kidney preparations, significant differences in functional characteristics of organic cation transport between various species have been reported. However, the underlying molecular mechanisms responsible for these interspecies differences are not known. The goal of this study was to determine the kinetics and substrate selectivities of organic cation transporter (OCT1) homologs from mouse, rat, rabbit, and human that may contribute to interspecies differences in the renal and hepatic handling of organic cations. With a series of n-tetraalkylammonium (nTAA) compounds, a correlation between increasing alkyl chain length and affinity for the four OCT1 homologs was observed. However, the apparent affinity constants (K(i)) differed among the species homologs. For the mouse homolog mOCT1, apparent K(i) values ranged from 7 microM for tetrabutylammonium to 2000 microM for tetramethylammonium. In contrast, the human homolog hOCT1 exhibited weaker interactions with the nTAA compounds. Trans-stimulation studies and current measurements in voltage-clamped oocytes demonstrated that larger nTAA compounds were transported at greater rates in oocytes expressing hOCT1, whereas smaller nTAAs were transported at greater rates in oocytes expressing mOCT1 or rOCT1. The rabbit homolog rbOCT1 exhibited intermediate properties in its interactions with nTAAs compared with its rodent and human counterparts. This report demonstrates that the human OCT1 homolog has functional properties distinct from those of the rodent and rabbit OCT1 homologs. The study underscores potential difficulties in extrapolating data from preclinical studies in animal models to humans.  (+info)

Characterization of MPP+ secretion across human intestinal Caco-2 cell monolayers: role of P-glycoprotein and a novel Na(+)-dependent organic cation transport mechanism. (8/255)

1. In the kidney, a number of transport proteins involved in the secretion of permanently charged organic cations have recently been cloned. To evaluate the possible similarities between intestine and kidney in the handling of organic cations we investigated the transport of 1-methyl-4-phenylpyridinium (MPP+) across monolayers of intestinal Caco-2 cells. MPP+ is a prototypic substrate of the cloned organic cation transporters hOCT1 and hOCT2. 2. In Caco-2 cell monolayers, the basolateral to apical flux of MPP+ was significantly greater than the apical to basolateral flux, consistent with net secretion of MPP+. 3. Net secretion of MPP+ was abolished by addition of either 10 microM cyclosporin A or 100 microM verapamil to the apical membrane. In contrast, secretion of MPP+ was unaffected by addition of either TEA (2 mM) or decynium-22 (2 microM) to either apical or basolateral membranes. These results suggest that MPP+ secretion is mediated primarily by P-glycoprotein located at the apical membrane. We found no evidence of a role for hOCT1 or hOCT2 in the secretion of MPP+. 4. In addition to net secretion of MPP+, we found evidence of a Na(+)-dependent MPP+ uptake mechanism at the apical membrane of Caco-2 cells. 5. Na(+)-dependent MPP+ uptake was sensitive to inhibition by the organic cations; decynium-22 (2 microM), TEA (2 mM) and cimetidine (5 mM) but not by carnitine, guanidine or proline. 6. These results suggest that net secretion of MPP+ across the apical membrane of Caco-2 cells is a function of the relative contributions of MPP+ secretion mediated by P-glycoprotein and MPP+ absorption mediated by a novel Na(+)-dependent transport mechanism.  (+info)

TY - JOUR. T1 - Involvement of nitric oxide/reactive oxygen species signaling via 8-nitro-cGMP formation in 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in PC12 cells and rat cerebellar granule neurons. AU - Masuda, Kumiko. AU - Tsutsuki, Hiroyasu. AU - Kasamatsu, Shingo. AU - Ida, Tomoaki. AU - Takata, Tsuyoshi. AU - Sugiura, Kikuya. AU - Nishida, Motohiro. AU - Watanabe, Yasuo. AU - Sawa, Tomohiro. AU - Akaike, Takaaki. AU - Ihara, Hideshi. PY - 2018/1/15. Y1 - 2018/1/15. N2 - To investigate the role of nitric oxide (NO)/reactive oxygen species (ROS) redox signaling in Parkinsons disease-like neurotoxicity, we used 1-methyl-4-phenylpyridinium (MPP+) treatment (a model of Parkinsons disease). We show that MPP+-induced neurotoxicity was dependent on ROS from neuronal NO synthase (nNOS) in nNOS-expressing PC12 cells (NPC12 cells) and rat cerebellar granule neurons (CGNs). Following MPP+ treatment, we found production of 8-nitroguanosine 3′,5′-cyclic monophosphate (8-nitro-cGMP), a ...
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces parkinsonism in humans after its oxidation into 1-methyl-4-phenylpyridinium ion (MPP+) by type B monoamine oxidase. The 1-amino analogues of MPTP and MPP+, 1-amino-4-phenyl-1,2,3, 6-tetrahydropyridine (APTP) and 1-amino-4-phenylpyridinium ion (APP+), were synthesized, and their cytotoxicity to clonal pheochromocytoma PC12 cells was examined using a tetrazolium formazan assay. After ...
Shop a large selection of Pyridines and derivatives products and learn more about 4-Phenylpyridine, 99%, ACROS Organics. 5g; Glass bottle.
My laboratory is interested in the molecular and cellular bases of neurological and neuropsychiatric disorders. For example, atypical dopamine function has been implicated in disorders such as Parkinsons disease, drug addiction, affective disorders and Schizophrenia. A current lab emphasis is in determining the mechanisms of cell death in Parkinsons disease. We are examining the biochemical and genetic events associated with parkinsonian models in vivo and in primary cultures of dopaminergic neurons. Microarray analysis is being used to globally determine which signaling pathways are utilized by parkinsonism-inducing agents as well as the known mutations. Enhanced understanding of the common and distinct cell death mechanisms associated with these toxins and genes may identify unique cellular targets for the generation of novel therapeutic interventions. In other studies, we are using homologous recombination and recombineering to create animal models in which gene expression in dopaminergic ...
My laboratory is interested in the molecular and cellular bases of neurological and neuropsychiatric disorders. For example, atypical dopamine function has been implicated in disorders such as Parkinsons disease, drug addiction, affective disorders and Schizophrenia. A current lab emphasis is in determining the mechanisms of cell death in Parkinsons disease. We are examining the biochemical and genetic events associated with parkinsonian models in vivo and in primary cultures of dopaminergic neurons. Microarray analysis is being used to globally determine which signaling pathways are utilized by parkinsonism-inducing agents as well as the known mutations. Enhanced understanding of the common and distinct cell death mechanisms associated with these toxins and genes may identify unique cellular targets for the generation of novel therapeutic interventions. In other studies, we are using homologous recombination and recombineering to create animal models in which gene expression in dopaminergic ...
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TY - JOUR. T1 - Protective effect of zizyphus spinachristi on mpp+-induced oxidative stress. AU - Singh, Vandita. AU - Essa, Mohamed Musthafa. AU - Guizani, Nejib. AU - Balakrishnan, Rengasamy. AU - Hemalatha, Tamiloli. AU - Manivasagam, Thamilarasan. AU - Justin-Thenmozhi, Arokiasamy. AU - Elangovan, Namasivayam. AU - Velusamy, Thirunavukkarasu. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Oxidative stress and mitochondrial dysfunction mediated neuro apoptosis is reported to play a major role in the pathology of Parkinsons disease. Zizyphus spina-christi fruits (ZSCF) are used as traditional medicines that are well-known for their high antioxidant properties. In the present study, we investigated the protective effects of ZSCF extract against 1-methyl-4-phenylpyridinium (MPP+) induced neurotoxicity in SH-SY5Y cell lines. The effect of ZCSF on MPP+ induced cell viability (MTT - 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay), membrane damage - (lactate dehydrogenase (LDH), oxidative ...
Long non-coding RNA small molecule RNA host gene 1 (SNHG1) was previously identified to be relevant with Parkinsons disease (PD) pathogenesis. This work aims to further elucidate the regulatory networks of SNHG1 involved in PD. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-hydrochloride (MPTP)-induced mice and 1-methyl-4-phenylpyridinium (MPP+)-treated SH-SY5Y cells were respectively constructed as the in vivo and in vitro PD models. Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCR. Protein expression levels of phosphate and tension homology deleted on chromosome ten (PTEN) were measured by western blotting assay. Cell viability and apoptosis were determined by MTT and flow cytometry assays. The interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis. Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. Overexpression of SNHG1 lowered viability
In view of the neurotoxic properties of 1-methyl-4-phenylpyridinium (MPP+), the monoamine oxidase-B-generated metabolite of the Parkinsonian agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (Kalgutkar et al., 2001), the identification of MPP+-like HPP+ and RHPP+ metabolites in significant quantities in the urine (Subramanyam et al., 1991b), plasma (Avent et al., 1997), and post-mortem brain samples (Eyles et al., 1997) in schizophrenic patients treated with HP is of neurotoxicological importance especially in the pathogenesis of HP-induced TD. Additional support for this proposal is evident from the observations that HPP+ displays MPP+-like neurotoxicity in vivo as well as in vitro (Bloomquist et al., 1994).. Although glucuronidation and reduced HP formation constitute the major routes of HP clearance in humans, the wide interindividual variations in HP oral clearance have been mainly attributed to the minor P450-catalyzed biotransformation pathways (30% of overall HP metabolism) (Kudo and ...
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Plasmid pDONR223-MPP5 from Dr. William Hahns lab contains the insert MPP5 and is published in Nature. 2010 Nov 24. ():. This plasmid is available through Addgene.
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4-hydroxy-4-methyl-2,5-cyclohexadien-1-one - chemical structural formula, chemical names, chemical properties, synthesis references
The organic cation transporter OCT1 (SLC22A1) mediates the uptake of vitamin B1, cationic drugs, and xenobiotics into hepatocytes. Nine percent of Caucasians lack or have very low OCT1 activity due to loss-of-function polymorphisms in OCT1 gene. Here we analyzed the global genetic variability in OCT1 to estimate the therapeutic relevance of OCT1 polymorphisms in populations beyond Caucasians and to identify evolutionary patterns of the common loss of OCT1 activity in humans. We applied massively parallel sequencing to screen for coding polymorphisms in 1,079 unrelated individuals from 53 populations worldwide. The obtained data was combined with the existing 1000 Genomes data comprising an additional 1,092 individuals from 14 populations. The identified OCT1 variants were characterized in vitro regarding their cellular localization and their ability to transport 10 known OCT1 substrates. Both the population genetics data and transport data were used in tandem to generate a world map of loss of OCT1
The organic cation transporter OCT1 (SLC22A1) mediates the uptake of vitamin B1, cationic drugs, and xenobiotics into hepatocytes. Nine percent of Caucasians lack or have very low OCT1 activity due to loss-of-function polymorphisms in OCT1 gene. Here we analyzed the global genetic variability in OCT1 to estimate the therapeutic relevance of OCT1 polymorphisms in populations beyond Caucasians and to identify evolutionary patterns of the common loss of OCT1 activity in humans. We applied massively parallel sequencing to screen for coding polymorphisms in 1,079 unrelated individuals from 53 populations worldwide. The obtained data was combined with the existing 1000 Genomes data comprising an additional 1,092 individuals from 14 populations. The identified OCT1 variants were characterized in vitro regarding their cellular localization and their ability to transport 10 known OCT1 substrates. Both the population genetics data and transport data were used in tandem to generate a world map of loss of OCT1
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Novel palladium(ii) and platinum(ii) complexes of 5,5-diethylbarbiturate (barb) with 2-phenylpyridine (Hppy), 2,2-bipyridine (bpy) and 2,2-dipyridylamine (dpya) have been prepared and characterized by elemental analysis, IR, UV-Vis, NMR and ESI-MS. Single-crystal diffraction measurements show that complex consists of binuclear [Pd2(μ-barb-κN,O)2(ppy-κN,C)2] moieties, while complexes are mononuclear, [M(barb-κN)2(L-κN,N)] (L = bpy or dpya). has a composition of [Pt(dpya-κN,N)2][Ag(barb-κN)2]2·4H2O and was assumed to have a structure of [Pt(barb-κN)(Hppy-κN)(ppy-κN,C)]·3H2O. The complexes were found to exhibit significant DNA binding affinity by a non-covalent binding mode, in accordance with molecular docking studies. In addition, complexes and displayed strong binding with supercoiled pUC19 plasmid DNA. Cellular uptake studies were performed to assess the subcellular localization of the selected complexes. A moderate radical scavenging activity of and was confirmed by DPPH and ABTS tests
Kidney-specific expression of human organic cation transporter 2 (OCT2/SLC22A2) is regulated by DNA methylation - BioChain Institute Inc.
Cerebellar granule cells are susceptible to the excitotoxin glutamate, which acts at N-methyl-D-aspartate (NMDA) receptors, as well as the neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+), the active cytotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Paradoxically, preincubation of cultured cerebellar granule cells with low concentrations of NMDA or glutamate markedly antagonizes the neurotoxicity resulting from subsequent exposure to toxic concentrations of either MPP+ or glutamate. The neuroprotective effects of NMDA and glutamate against MPP+ toxicity are observed at agonist concentrations as low as 1 microM, are blocked by specific NMDA receptor antagonists, and require at least 30 min to develop fully. Moreover, NMDA receptor-mediated neuroprotection is prevented by the RNA synthesis inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide. Thus, in cerebellar granule cells activation of NMDA receptors by glutamate can result in either ...
We have previously demonstrated the unexpected neuroprotection of the anti-cancer agent SU4312 in cellular models associated with Parkinsons disease (PD). However, the precise mechanisms underlying its neuroprotection are still unknown, and the effects of SU4312 on rodent models of PD have not been characterized. In the current study, we found that the protection of SU4312 against 1-methyl-4-phenylpyridinium ion (MPP(+))-induced neurotoxicity in PC12 cells was achieved through the activation of transcription factor myocyte enhancer factor 2D (MEF2D), as evidenced by the fact that SU4312 stimulated myocyte enhancer factor 2 (MEF2) transcriptional activity and prevented the inhibition of MEF2D protein expression caused by MPP(+), and that short hairpin RNA (ShRNA)-mediated knockdown of MEF2D significantly abolished the neuroprotection of SU4312 ...
A thin film of triphenylamine dimer, N,N′-bis(3-methylphenyl)-N,N′-bis(phenyl)-benzidine (TPD), doped with fac tris(2-phenylpyridine) iridium (Ir(ppy)3) and platinum octaethyl porphine (PtOEP) is char
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Within SWECLIM a 3D fully coupled ice-ocean model has been developed based on the massively parallel OCCAM code from Southampton. Compared to the global OCCAM the model has to be adopted to Baltic Sea conditions with implementations of high-frequent atmospheric forcing fields in connection with adequate bulk formulae for wind stress, heat uxes and freshwater uxes, solar radiation, river runoff, active open boundary conditions, a second-order moment turbulence closure scheme and a dynamic-thermodynamic sea ice model. Thereby, state-of-the-art sub-models and parameterizations have been used. RCO is the first 3D coupled ice-ocean model for the Baltic Sea with the above mentioned specifications suitable for use on mpp computers like CRAY-T3Es. Thus, a milestone for 3D ocean model development has been set. No other model is as fast as RCO. The performance has been improved significantly using advanced algorithms to optimize processor maps. This guarantees work load balance between the different ...
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5-chloro-2-methyl-4-nitroaniline chemical properties, What are the chemical properties of 5-chloro-2-methyl-4-nitroaniline 13852-51-2, What are the physical properties of 5-chloro-2-methyl-4-nitroaniline ect.
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ethyl (2E,4E,6E,8E)-3-methyl-9-phenyl-2,4,6,8-nonatetraenoate - chemical structural formula, chemical names, chemical properties, synthesis references
You are viewing an interactive 3D depiction of the molecule (2z)-5-bromo-5-methyl-3-phenyl-2-(phenylimino)-1,3-thiazinan-4-one (C17H15BrN2OS) from the PQR.
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DESCRIPTION (provided by applicant): Depression and related disorders are a major public health problem, compounded by the fact that at least half of patients are not effectively treated by currently available medications. Among the most commonly prescribed is the class of selective serotonin (5-HT) reuptake inhibitors (SSRIs), which act to inhibit 5-HT transporter (SERT) mediated 5-HT uptake. The increase in extracellular 5-HT that follows is thought to be critical for initiation of the cascade of downstream events needed for therapeutic effects. Although SERT is the major player regulating high-affinity 5-HT uptake, there is emerging evidence for an important role of organic cation transporter-3 (OCT3) and possibly the plasma membrane monoamine transporter (PMAT) in taking up 5-HT in brain. This raises the possibility that lack of therapeutic response following SERT blockade could be due to significant 5-HT uptake by OCT3 (and/or PMAT). Our studies using decynium-22 (D-22), a blocker of both ...
TY - JOUR. T1 - Targeted disruption of organic cation transporter 3 (Oct3) ameliorates ischemic brain damage through modulating histamine and regulatory T cells. AU - Zhu, Pengxiang. AU - Hata, Ryuji. AU - Ogasawara, Masahito. AU - Cao, Fang. AU - Kameda, Kenji. AU - Yamauchi, Kohei. AU - Schinkel, Alfred H.. AU - Maeyama, Kazutaka. AU - Sakanaka, Masahiro. N1 - Copyright: Copyright 2013 Elsevier B.V., All rights reserved.. PY - 2012/10. Y1 - 2012/10. N2 - The organic cation transporters OCT1, 2, and 3 (SLC22A1-3) have been implicated in the elimination of biogenic amines such as histamine. Among them, OCT3 was identified as an uptake-2 transporter, responsible for clearance of histamine. Because increasing evidence suggests the involvement of histamine in cerebral ischemia, we investigated the effects of targeted disruption of organic cation transporter-3 (Oct3) on the severity of ischemic brain damage. Transient focal ischemia for 1 hour was induced by occlusion of the middle cerebral artery ...
Solute carrier family 22 member 3 (SLC22A3) also known as the organic cation transporter 3 (OCT3) or extraneuronal monoamine transporter (EMT) is a protein that in humans is encoded by the SLC22A3 gene.[1][2][3] Polyspecific organic cation transporters in the liver, kidney, intestine, and other organs are critical for elimination of many endogenous small organic cations as well as a wide array of drugs and environmental toxins. This gene is one of three similar cation transporter genes located in a cluster on chromosome 6. The encoded protein contains twelve putative transmembrane domains and is a plasma integral membrane protein.[3] ...
In myocardial ischemia, adrenergic terminals undergo ATP depletion, hypoxia, and intracellular pH reduction, causing the accumulation of axoplasmic norepinephrine (NE) and intracellular Na+ [via the Na+-H+ exchanger (NHE)]. This forces the reversal of the Na+- and Cl−-dependent NE transporter (NET), triggering massive carrier-mediated NE release and, thus, arrhythmias. We have now developed a cellular model of carrier-mediated NE release using an LLC-PK1 cell line stably transfected with human NET cDNA (LLC-NET). LLC-NET cells transported [3H]NE and [3H]N-methyl-4-phenylpyridinium ([3H]MPP+) in an inward direction. This uptake was abolished by the NET inhibitors desipramine (100 nM) and mazindol (300 nM) and by extracellular Na+ removal. Na+-gradient reversal induced an efflux of3H-substrate from preloaded LLC-NET cells. Desipramine and mazindol blocked this efflux. Because of its greater intracellular stability and higher sensitivity to Na+-gradient reversal, [3H]MPP+ proved preferable to ...
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DESCRIPTION (provided by applicant): This project aims to demonstrate that the evolution of plant biosynthetic pathways can be accelerated and driven to favor the synthesis of ligands which interact with a specific human target protein. This is achieved bysubjecting mutant plant cells to selection pressures favoring the survival of mutants with the phenotype of interest. As an example, this approach will be used to optimize pharmacological activity in Lobelia cardinalis, which inhibits the human dopamine transporter (hDAT), putatively by its ability to synthesize the complex alkaloid, lobinaline. A stable transgenic line of L. cardinalis plant cells expressing the hDAT has been established. These cells show increased sensitivity to toxins transported into the cell by the hDAT, including the neurotoxin MPP+. A large, genetically diverse, population of gain-of-function mutants expressing the hDAT has now been generated, and selected on medium containing 100uM MPP+, which kills the vast majority of ...
Red shift of green-emission band has been observed for fac tris(2-phenylpyridine) iridium (Ir(ppy)3) doped in polycarbonate at 8 K during time evolution after 355-nm laser of 1-ns pulse width. We explain the peak shift and vibronic structure of the emission band using the Franck-Condon principle and the model of (1) three zero-field splitting substates of the triplet state, (2) relaxation processes among the three substates, and (3) different Huang-Rhys factors for these substates. Good agreement was obtained between the calculated and measured emission spectra at various delay times.. © 2005 Chinese Optics Letters. PDF Article ...
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CAS NO:896465-66-0; Chemical name:1-Isoamyl-2-methyl-3,3-dibenzyl-5-chloroindolium bromide ; physical and chemical property of 896465-66-0, 1-Isoamyl-2-methyl-3,3-dibenzyl-5-chloroindolium bromide is provided by ChemNet.com
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Aldrich-359505; 7-Methyl-1,5,7-triazabicyclo[4.4.0]dec-5-ene 0.98; CAS No.: 84030-20-6; Synonyms: 1,3,4,6,7,8-Hexahydro-1-methyl-2H-pyrimido[1,2-a]pyrimidine; MTBD; Linear Formula: C8H15N3; Empirical Formula: C8H15N3; find related products, papers, technical documents, MSDS & more at Sigma-Aldrich.
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5-methyl-2-oxooxolane-3-carboxylic acid; CAS Number: 25277-91-2; find Enamine-ENAH5802E785 MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich
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Derivatives of (1.1)ferrocenophane, which carry a reactive olefin function at one of the bridges, are useful in attaching the ferrocenophane system to v...
The industrial synthesis of MPP+ for sale as the herbicide cyperquat used methyl chloride as the source of the methyl group. ... MPP+ (1-methyl-4-phenylpyridinium) is a positively charged organic molecule with the chemical formula C12H12N+. It is a ... Zhang Y, Zhou TY, Zhang KD, Dai JL, Zhu YY, Zhao X (June 2014). "Encapsulation enhanced dimerization of a series of 4-aryl-N- ... 18 (4): 409-14. doi:10.1089/jmf.2014.3241. PMID 25325362. Hassan MN, Thakar JN, Grimes JD (1987). "Cyperquat (MPP+), but not ...
doi:10.1385/1-59259-365-8:133 Lannuzel, A. and Michel, P. P. (2008). Atypical Parkinsonism in the French West Indies: The Plant ... 63 (4): 1053-1056. doi:10.1021/jf504500g. PMID 25594104. Potts, L. F.; Luzzio, F. A.; Smith, S. C.; Hetman, M; Champy, P; ... 33 (1): 53-8. doi:10.1016/j.neuro.2011.10.009. PMID 22130466. Le Ven, J.; Schmitz-Afonso, I.; Touboul, D.; Buisson, D.; Akagah ... 88 (1): 63-69. doi:10.1046/j.1471-4159.2003.02138.x. PMID 14675150. S2CID 24056913. (Chemical articles with multiple compound ...
Accessed 10:46PM, 4/13/07. www.mc.vanderbilt.edu/root/vumc.php?site=granner&doc=119 Burgess SC, He T, Yan Z, Lindner J, Sherry ... 98 (1): 77-91. doi:10.1093/aob/mcl096. PMC 2803547. PMID 16704997. Chen ZH, Walker RP, Técsi LI, Lea PJ, Leegood RC (May 2004 ... 1697 (1-2): 271-8. doi:10.1016/j.bbapap.2003.11.030. PMID 15023367. Trapani S, Linss J, Goldenberg S, Fischer H, Craievich AF, ... 59 (1): 105-13. doi:10.1016/j.jhep.2013.02.020. PMC 3910155. PMID 23466304. Chakravarty K, Cassuto H, Reshef L, Hanson RW (2005 ...
Retrieved 4 November 2013. Kleiman, Mark A.R.; Hawdon, James E. (2011). Encyclopedia of Drug Policy. Thousand Oaks: Sage ... 1-Methyl-4-phenylpyridinium (MPP+), a metabolite of MPTP, causes rapid onset of irreversible symptoms similar to Parkinson's ... ISBN 978-92-1-148277-5. Retrieved 9 January 2017. The National Drug Control Strategy: 2000 Annual Report. Washington, D.C.: ... 1 (4): 36-39. Retrieved 23 March 2018. "Club Drugs". National Institute on Drug Abuse. Retrieved 9 January 2017. "Department of ...
46 (4): 598-605. doi:10.1002/1531-8249(199910)46:4. 3.0.CO;2-F. PMID 10514096. Farrer M, Chan P, Chen R, Tan L, Lincoln S, ... 281 (4): 341-6. doi:10.1001/jama.281.4.341. PMID 9929087. Langston JW, Forno LS, Tetrud J, Reeves AG, Kaplan JA, Karluk D (Oct ... 107 (4): 481-5. doi:10.7326/0003-4819-107-4-481. PMID 3631786. Ricaurte GA, Forno LS, Wilson MA, DeLanney LE, Irwin I, Molliver ... 7 (1): 2-13. doi:10.1002/mds.870070103. PMID 1557062. S2CID 31485426. Widner H, Tetrud J, Rehncrona S, Snow B, Brundin P, ...
Structural analogs of desmethylprodine with different N-substituents than a methyl group on the piperidine have been ... 13 (4): 367-74. doi:10.1016/0376-8716(84)90004-8. PMID 6148225. Davis GC, Williams AC, Markey SP, Ebert MH, Caine ED, Reichert ... Desmethylprodine or 1-methyl-4-phenyl-4-propionoxypiperidine (MPPP, Ro 2-0718) is an opioid analgesic drug developed in the ... It was later found that his development of Parkinson's was due to a common impurity in the synthesis of MPPP called MPTP (1- ...
In all known secalonic acids, the methyl and methoxycarbonyl substituents are found to be trans to each other, and X-ray ... 713 (1-3): 58-67. doi:10.1016/j.ejphar.2013.04.029. ISSN 0014-2999. PMID 23665112. Millot M, Tomasi S, Studzinska E, Rouaud I, ... 58 (1): 85-91. doi:10.1016/j.neuint.2010.10.016. PMID 21073911. Zhai, Aifeng; Zhu, Xiaonan; Wang, Xuelan; Chen, Ruzhu; Wang, ... The 2-2'linked secalonic acid A isomerizes in DMSO at room temperature to the 2-4'linked secalonic acid A and 4-4'linked ...
In the simplest case of a single-substrate enzyme obeying Michaelis-Menten kinetics, the typical scheme E + S ⇌ k − 1 k 1 ES → ... Cells in the central nervous system (astrocytes) include MAO-B that oxidizes MPTP to 1-methyl-4-phenylpyridinium (MPP+), which ... After an accidental ingestion of a contaminated opioid drug desmethylprodine, the neurotoxic effect of 1-methyl-4-phenyl-1,2,3, ... Competitive substrates, such as 4-substituted benzaldehydes for mushrooms, compete with the substrate lowering the amount of ...
"1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine". ChemIDplus. Frim, D. M.; Uhler, T. A.; Galpern, W. R.; Beal, M. F.; Breakefield ... MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a prodrug to the neurotoxin MPP+, which causes permanent symptoms of ... 1 (3): 249-254. doi:10.1016/0165-1781(79)90006-4. PMID 298352. S2CID 44304872. "Success reported using fetal tissue to repair a ... 2 (1): 141-151. doi:10.1038/nprot.2006.342. PMID 17401348. S2CID 39743261. "Pesticides and Parkinson's Disease - A Critical ...
84 (1): 43-52. doi:10.1046/j.1471-4159.2003.01566.x. PMID 12485400. Stiel H, Daehne S, Teuchner K. J-aggregates of ... Decynium-22 has been shown to block the uptake of the neurotoxin 1-methyl-4-phenylpyridinium (MPP) via the OCT3 transporter in ... Dynamics of formation of 1,1′-diethyl-2,2′-cyanine iodide J-aggregates in solution. J Physical Chem A. 2000;104:9670-9674. ... 2010). "Membrane potential and pH-dependent accumulation of decynium-22 (1,1′-diethyl-2,2′-cyanine iodide) fluorescence through ...
Table 1 represents a summary of the PD animal models and details regarding their mechanisms of action, pathogenesis, and ... ISBN 978-1-259-64115-2. Hatcher, Jaime M.; Pennell, Kurt D.; Miller, Gary W. (June 2008). "Parkinson's disease and pesticides: ... Braak staging is a widely used method to measure the stage of pathology (stage 1 being the lowest level of pathology and stage ... Protein Deglycase (DJ-1) mutations are associated with recessive forms of familial parkinsonism. It is a molecular chaperone ...
... methyl ester MeSH D03.383.725.210 - dimethindene MeSH D03.383.725.220 - 2,2'-dipyridyl MeSH D03.383.725.227 - disopyramide MeSH ... methyl ester MeSH D03.383.725.547.950 - xanthinol niacinate MeSH D03.383.725.565 - nicotinyl alcohol MeSH D03.383.725.592 - ... 5-tetrahydro-8-chloro-3-methyl-5-phenyl-1h-3-benzazepin-7-ol MeSH D03.438.079.800 - 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl- ... alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid MeSH D03.383.129.385.162 - cycloserine MeSH D03.383.129.385.231 - ...
27 (4): 1064-74. doi:10.1002/hep.510270423. PMID 9537447. S2CID 11899686. Yang H, Zhou L, Shi Q, Zhao Y, Lin H, Zhang M, Zhao S ... 22 (1-6): 190-4. doi:10.1159/000130933. PMID 752471. Pol S, Bousquet-Lemercier B, Pavé-Preux M, Bulle F, Passage E, Hanoune J, ... 832 (1): 46-51. doi:10.1016/0167-4838(85)90172-4. PMID 4052435. Davidson RG, Cortner JA, Rattazzi MC, Ruddle FH, Lubs HA (Jul ... 138 (1-2): 171-4. doi:10.1016/0378-1119(94)90802-8. PMID 8125298. Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, Suyama A, Sugano ...
Phenylethylamine (10), amphetamine [AMPH (11 & 12)], methylenedioxy methamphetamine [METH (13)] and N-methyl-4-phenylpyridinium ... 16 (1): 9-18. doi:10.1016/0031-9422(77)83004-5. Lynnes T, Horne SM, Prüß BM (2014). "ß-Phenylethylamine as a novel nutrient ... 2015 Oct; 34: 1-7. Published online 2015 Jan 20. doi: 10.1016/j.conb.2015.01.001 Broadley KJ (March 2010). "The vascular ... 96 (1): 165-71. doi:10.1016/j.meatsci.2013.06.030. PMID 23896151. Acetoacetic acid (AAA) and ß-phenylethylamine (PEA) performed ...
Phenylethylamine Amphetamine MDMA N-Methyl-4-phenylpyridinium (MPP+) (very potent inhibitors of VMAT2 mediated serotonin ... 31 (4): 483-19. doi:10.1002/med.20187. PMC 3019297. PMID 20135628. Liu Y, Peter D, Rogahani A, Schuldiner S, Prive GG, ... 31 (4): 483-519. doi:10.1002/med.20187. PMC 3019297. PMID 20135628. Henry J. P.; Botton D.; et al. (1994). "Biochemistry and ... 1216 (1): 86-98. Bibcode:2011NYASA1216...86E. doi:10.1111/j.1749-6632.2010.05906.x. PMC 4183197. PMID 21272013. VMAT2 is the ...
Kalgutkar AS, Nguyen HT (September 2004). "Identification of an N-methyl-4-phenylpyridinium-like metabolite of the ... Guarino B (4 May 2016). "Abuse of diarrhea medicine you know well is alarming physicians". Washington Post. Retrieved 6 May ... 69 (1): 83-86. doi:10.1016/j.annemergmed.2016.03.047. PMID 27140747. Mukarram O, Hindi Y, Catalasan G, Ward J (2016). " ... ISBN 978-92-1-130230-1. Archived from the original on 8 September 2017. US patent 5612054, Jeffrey L. Garwin, "Pharmaceutical ...
For example, rotenone, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its active metabolite 1-methyl-4- ... phenylpyridinium (MPP+), and 6-hydroxydopamine (6-OHDA), have been shown to induce dopaminergic cell death in vivo and in vitro ... Distinct Effects of Rotenone, 1-methyl-4-phenylpyridinium and 6-hydroxydopamine on Cellular Bioenergetics and Cell Death ...
Ramelteon ameliorated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in neuronal cells in … ... Korean red ginseng decreases 1-methyl-4-phenylpyridinium-induced mitophagy in SH-SY5Y cells. ...
1-methyl-4-phenylpyridinium ([(3)H]MPP(+)) by Xenopus laevis oocytes injected with mOCT1 (Slc22a1) or mOCT2 (Slc22a2) cRNA was ... Mari Kakehi 1 , Noriko Koyabu, Takanori Nakamura, Takeshi Uchiumi, Michihiko Kuwano, Hisakazu Ohtani, Yasufumi Sawada ... 1 Department of Medico-Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, ... 1-methyl-4-phenylpyridinium ([(3)H]MPP(+)) by Xenopus laevis oocytes injected with mOCT1 (Slc22a1) or mOCT2 (Slc22a2) cRNA was ...
Preimplantation Embryonic Lethality 1 (ortholog); FOUND IN cell cortex (ortholog); cytoplasm (ortholog); nucleus (ortholog); ... N-methyl-4-phenylpyridinium increases expression. EXP. 6480464. 1-Methyl-4-phenylpyridinium results in increased expression of ... Orthologs 1. Homo sapiens (human):. TLE6 (TLE family member 6, subcortical maternal complex member). HGNC. EggNOG, Ensembl, ... 1. 27829089. Rat. 7411566. Bw136. Body weight QTL 136. 10.4. 0.001. body mass (VT:0001259). body weight gain (CMO:0000420). 7. ...
1-methyl-4-phenylpyridinium. NMN. N1-methylnicotinamide. PAH. p-aminohippuric acid. dopa. 3, 4-dihydroxyphenylalanine. PBS. ... The IC50 was estimated by a sigmoidal inhibition model and was fit to the equationV = V0/(1 + (I/IC50)n) by nonlinear ... 4). The endogenous uptake of cimetidine was moderate (6.84 vs. 2.12 pmol/mg protein/μM for cimetidine vs. TEA uptake at 30 min ... The final mixture (1 ml) was applied to each well after rinsing the cells with the Opti-MEM media once. The cells were exposed ...
... affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not ... 3, 4] Exposure to the weed killer paraquat or to the fungicides maneb or mancozeb is particularly toxic, increasing the risk ... 3, 4] Increased PD risk was also associated with proxy conditions of exposure to organic pollutants, such as farming, well- ... MPTP crosses the blood-brain barrier and is oxidized to 1-methyl-4-phenylpyridinium (MPP+) by monoamine oxidase (MAO)-B. [6] ...
In DA neurons, a battery of enzymes, including monoamine oxidases, ALDHs, and catechol-O-methyl transferases, are used to ... Guoxiang Liu,1 Jia Yu,1 Jinhui Ding,2 Chengsong Xie,1 Lixin Sun,1 Iakov Rudenko,1 Wang Zheng,1 Namratha Sastry,1 Jing Luo,3 Gay ... 6-methyl-2-phenylazo-3-pyridinol (SIB1757) (26), also significantly improved the survival of TH-positive neurons in A53T ... We found that Aldh1a1+/+ and Aldh1a1-/- midbrain DA neurons showed no difference in 1-methyl-4-phenylpyridinium+- (MPP+-), ...
1), 153-159. [Google Scholar] [CrossRef] [PubMed]. *Kann, O.; Kovacs, R. Mitochondria and neuronal activity. Am. J. Physiol. ... 1. Introduction. Mitochondria are organelles that can be found in most eukaryotic cells and are required for a wide range of ... Figure 1. Schematic depiction of mitochondrial dynamics in mammalian cells. (A) Cytosolic Drp1 is recruited to the ... Figure 1. Schematic depiction of mitochondrial dynamics in mammalian cells. (A) Cytosolic Drp1 is recruited to the ...
Lu Yao, Wenming Li, Hua She, Juan Dou, Leili Jia, Yingli He, Qian Yang, Jinqiu Zhu, Natalie L. Cápiro, Douglas I. Walker, Kurt D. Pennell, Yuanping Pang, Yong Liu, Yifan Han, Zixu Mao ...
Anthony J. Atala ORCID: orcid.org/0000-0001-8186-21601 Show authors. Scientific Reports volume 10, Article number: 9766 (2020) ... Figure 4. Cytokine production and the effect of exogenous cytokines. In A and B, two groups of 50 organoids each were pooled ... Figure 1. Hypoxia induced permeability and cell death. (A) Zo-1 staining around the organoid showing complete BBB coverage ... Zona occludin 1 (ZO-1) and occludin expression were increased under hypoxic (480 pg/ml and 1.7 ng/ml) compared to normoxic ...
... affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not ... It is recommended to begin therapy with a single 1-mg dose. Dosage can be titrated by 1 mg each week or so, until a total of 4- ... Stated another way, in a delayed-start design, half of the subjects in the study take the trial drug from day 1 and the other ... 75] Over 18 months, rasagiline 1 mg/day started early resulted in less worsening in mean total UPDRS score than when it was ...
4A) (note: KO cells are a bit more sensitive to H2O2) or glutamate (data not shown), and displayed no enhancement of β(III)- ... n = 4; *p , 0.05). B, ad-GFP- and ad-Nrf2-GFP (50 MOI)-infected cultures were observed for ARE activation in primary cultures ... Figure 4. In Nrf2 KO cultures, in which the effect of tBHQ on ARE activity is lost, neuronal protection is abrogated. A, ... 1A) and sulforaphane (B) induced a dramatic, dose-dependent increase in hPAP activity. The mRNA levels for ARE-driven hPAP, ...
The aims of the present study are (1) to investigate whether naturally occurring S-enantiomer of ar-turmerone (S-Tur) protects ... They used the BV2 microglial cell line and midbrain slice cultures to 1) determine if ar-turmerone suppresses dopaminergic ... Additionally, two analogs more potently inhibited dopaminergic neurodegeneration triggered by a neurotoxin, 1-methyl-4- ... phenylpyridinium, than S-Tur. Taken together, we identified two ar-turmerone analogs that directly and potently protected ...
Neurotoxins; Methyl-compounds; Laboratory-animals; Laboratory-testing; Chemical-structure; Neurological-reactions; Neurological ... 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a pro-neurotoxicant that must be metabolized to 1-methyl-4- ... phenylpyridinium (MPP+) and taken up into striatal dopaminergic neurons to produce neurodegeneration. Recently, we showed wide ...
RT-PCR analysis shows the upregulation of inducible nitric oxide synthase, interleukin-1,i,β,/i,, and tumor necrosis ... could contribute to the survival of nigrostriatal dopamine neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) ... MAC-1) or glial fibrillary acidic protein (GFAP) immunocytochemistry, respectively. ... Figure 1(c); ) and a reduction of the density of TH+ fibers in the striatum (Figure 3(b); ) compared to the MPTP- and CAP- ...
CBR-470-1 neuroprotection is dependent upon Nrf2, as Nrf2 shRNA or CRISPR/Cas9-mediated Nrf2 knockout, abolished CBR-470-1- ... Treatment of SH-SY5Y cells with CBR-470-1, an inhibitor of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1), leads to ... In Keap1 or PGK1 knockout SH-SY5Y cells,CBR-470-1 failed to offer further cytoprotection against MPP+. Collectively PGK1 ... Consistent with these findings, PGK1 depletion or knockout mimicked CBR-470-1-induced actions and rendered SH-SY5Y cells ...
1. 4. Not Yet Recruiting. Treatment. Advanced Ovarian Cancer / Epithelial Ovarian Cancer / Ovarian Cancer / Stage III Ovarian ... 1038915-60-4. InChI Key. PCHKPVIQAHNQLW-CQSZACIVSA-N. InChI. InChI=1S/C19H20N4O/c20-19(24)17-5-1-3-15-12-23(22-18(15)17)16-8-6- ... Selectivity towards PARP-1 and PARP-2 is 100-fold higher than for other PARP family members.2 Niraparib-induced cytotoxicity ... 1. 4. Recruiting. Prevention. Adult Patients With Platinum-sensitive, Relapsed, High Grade Serous Epithelial Ovarian Cancer. 1 ...
1]. Hong-xiao Li, Ling Shi, Shang-jie Liang Chen-chen Fang, Qian-qian Xu, Ge Lu, Qian Wang, Jie Cheng, Jie Shen, Mei-hong Shen ... Cai-lian Fana, 1, Wan-jun Caib, 1, Meng-nan Yeb, Miao Chenb, Yi Daib. ... Journal of Chinese Integrative Medicine, 2008, 6(1): 31 [7]. Yi-ting He, Qing-lin Zha, Jian-ping Yu, Yong Tan, Cheng Lu, Ai- ... Journal of Chinese Integrative Medicine, 2008, 6(1): 107-110 [3]. Jin-zhou Tian, Jing Shi, Xin-qing Zhang, Qi Bi, Xin Ma, Zhi- ...
Chen, S-Y., Hsu, H. L., Lin, J. J., 余明治(Ming-Chi Y, 江玲玲(Ling-Ling C & 李俊年(Chun-Nie L, 2010, In: 呼吸治療. 9, 1, p. 1-12 12 p.. ... Hou, Y. C., Lu, C. L., Zheng, C. M., Liu, W. C., Yen, T. H., Chen, R. M., Lin, Y. F., Chao, C. T. & Lu, K. C., Apr 1 2020, In: ... Chen, M., Huang, Y. C., Ko, I. L., Yang, S., Chang, Y. H., Huang, W. J. S. & Chen, Y. M. A., Sep 1 2009, In: Urology. 74, 3, p ... Chen, W. C., Chou, W. H., Chu, H. W., Huang, C. C., Liu, X., Chang, W. P., Chou, Y. H. & Chang, W. C., Dec 1 2019, In: ...
Requirement of a dopaminergic neuronal phenotype for toxicity of low concentrations of 1-methyl-4-phenylpyridinium to human ... Published in: Toxicology and Applied Pharmacology ; 241 (2009), 1. - pp. 23-35. - ISSN 0041-008X. - eISSN 1096-0333 ...
Y1 - 2006/8/1. N2 - A cDNA coding a new H+/organic cation antiporter, human kidney-specific multidrug and toxin extrusion 2 ( ... hMATE2-K also transported cimetidine, 1-methyl-4-phenylpyridinium (MPP), procainamide, metformin, and N 1-methylnicotinamide. ... hMATE2-K also transported cimetidine, 1-methyl-4-phenylpyridinium (MPP), procainamide, metformin, and N 1-methylnicotinamide. ... hMATE2-K also transported cimetidine, 1-methyl-4-phenylpyridinium (MPP), procainamide, metformin, and N 1-methylnicotinamide. ...
N Methyl 4 phenylpyridine N-Methyl-4-phenylpyridine N-Methyl-4-phenylpyridinium ... N Methyl 4 phenylpyridine. N-Methyl-4-phenylpyridine. N-Methyl-4-phenylpyridinium. ... 1-Methyl-4-phenylpyridinium - Preferred Concept UI. M0023993. Scope note. An active neurotoxic metabolite of 1-METHYL-4-PHENYL- ... 1-Methyl-4-phenylpyridinium Entry term(s). 1 Methyl 4 phenylpyridine 1 Methyl 4 phenylpyridinium 1 Methyl 4 phenylpyridinium ...
2019: 1-6.. [14]. Caballero M, Amiri S, Denney JT, Monsivais P, Hystad P, Amram O. Estimated Residential Exposure to ... 4]. Kaur K, Kaur R. Occupational Pesticide Exposure, Impaired DNA Repair, and Diseases. Indian J Occup Environ Med. 2018 22: 74 ... 1]. Ball N, Teo WP, Chandra S, Chapman J. Parkinsons Disease and the Environment. Front Neurol. 2019 10: 218. ... 2010 20 Suppl 1: S221-238.. [31]. Hu G, Bidel S, Jousilahti P, Antikainen R, Tuomilehto J. Coffee and tea consumption and the ...
A study of the elimination of water from lithium-cationized tripeptide methyl esters by means of tandem mass spectrometry and ... A study on the mechanism of the Parkinsonian-causing drug 1-methyl-4-phenylpyridinium (MPP+)  Samms, Warren C.; Perera, Rohan ... Substituted 3-oxo-1,2,5-thiadiazolidine 1,1-dioxides: a new class of potential mechanism-based inhibitors of human leukocyte ... A series of substituted 3-oxo-1,2,5-thiadiazolidine 1,1-dioxides has been synthesized and their in vitro inhibitory activity ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
Syb-prII-1 is a ß-type scorpion neurotoxin isolated from the scorpion venom of Buthus martensi Karsch (BmK). It has an ... After Syb-prII-1 was given, the phosphorylation level of the mitogen-activated protein kinases (MAPKs) pathway showed a dose- ... Moreover, Syb-prII-1(4.0 mg/kg) could significantly change the steady-state activation and inactivation curves of Nav1.8. The ... A 2 1/2-day interactive system dynamics workshop involving experts across multiple disciplines was convened to develop the ...
2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 1,2-Benzoquinones use Benzoquinones 1,2-Cyclic-Inositol-Phosphate Phosphodiesterase use Glycerophosphoinositol ... 1-Acylglycerol-3-Phosphate O-Acyltransferase 1-Acylglycerophosphocholine Acyltransferase use 1-Acylglycerophosphocholine O- ... 3-Phosphoshikimate 1-Carboxyvinyltransferase 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl) ...
  • The neurotoxin MPP + (1-methyl-4-phenylpyridinium ion) disrupts mitochondrial function leading to oxidative stress and neuronal death. (aging-us.com)
  • Paraquat, a herbicide with molecular similarities to MPP+ (1-methyl-4-phenylpyridinium, a metabolite of the neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)), is among the earliest and most well studied pesticides linked to an increased risk of developing PD. (researchsquare.com)
  • MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydro pyridine ) is a neurotoxin that causes permanent symptoms of Parkinson's disease by killing certain neurons in the substantia nigra of the brain. (chemeurope.com)
  • 1985. Spin-trapping of methyl radical in the oxidative metabolism of 1,2-dimethylhydrazine. (cdc.gov)
  • Pretreatment with CBR-470-1 potently attenuated MPP + -induced oxidative injury and SH-SY5Y cell apoptosis. (aging-us.com)
  • Paraoxonase (PON)-1 Activity in Overweight and Obese Children and Adolescents: Association with Obesity-Related Inflammation and Oxidative Stress. (researchgate.net)
  • Oxidative stress and mitochondrial dysfunction are major events that occur during neuronal death that causes PD [ 4,5 ]. (avensonline.org)
  • Herein, we evaluated the anti-inflammatory and antioxidant efficacy of diapocynin, an oxidative metabolite of the naturally occurring agent apocynin, in a pre-clinical 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. (springer.com)
  • Nigral tyrosine hydroxylase (TH)-positive neurons as well as oxidative markers 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE) and striatal dopamine levels were quantified for assessment of the neuroprotective efficacy of diapocynin. (springer.com)
  • Notably, diapocynin markedly inhibited MPTP-induced oxidative markers including 3-NT and 4-HNE levels in the SN. (springer.com)
  • Exposure to the chemical 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) can lead to the presence of its toxic metabolite, 1-methyl-4-phenylpyridinium (MPP+), in the brain, which induces a selective destruction of dopaminergic nigrostriatal neurons and the occurance of Parkinson's disease. (ntu.edu.tw)
  • Fuchs e, or downloading a drug, kahn da neurotoxins 1-methyl-4-phenyl-pyridinium ion, which cookies to pay without physician if you. (blazingquarters.com)
  • RT-PCR analysis shows the upregulation of inducible nitric oxide synthase, interleukin-1 β , and tumor necrosis factor- α in microglia in the SN in vivo, indicating the activation of the inflammatory system. (hindawi.com)
  • Neuroinflammatory markers, such as ionized calcium binding adaptor molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), gp91phox and inducible nitric oxide synthase (iNOS), were measured in the nigrostriatal system. (springer.com)
  • We characterized the function of mouse organic cation transporter OCT2 (TC 2.A.19.1.5) in comparison with that of OCT1 (TC 2.A.19.1.1). (nih.gov)
  • Transient receptor potential vanilloid subtype 1 (TRPV1), a polymodal and nonselective cation channel, is activated by a number of endogenous and exogenous stimuli, including natural vanilloids (capsaicin and resiniferatoxin), heat, acids, and endocannabinoids such as anandamide (AEA) [ 8 , 9 ]. (hindawi.com)
  • Once inside the brain, MPTP is metabolized into the toxic cation 1-methyl-4-phenylpyridinium (MPP+) by the enzyme MAO-B of glial cells. (chemeurope.com)
  • ClC-1 is a member of a large family of voltage-gated chloride channels, abundantly expressed in human skeletal muscle. (inforang.com)
  • In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to produce the proposed sensitization and precipitating stages and determine if curcumin can ameliorate the toxic changes. (avensonline.org)
  • MPTP induced a significant loss of nigrostriatal dopamine neurons and glial activation in the substantia nigra (SN) and striatum (STR) as visualized by tyrosine hydroxylase (TH) or macrophage antigen complex-1 (MAC-1) or glial fibrillary acidic protein (GFAP) immunocytochemistry, respectively. (hindawi.com)
  • TLR4 signaling mediated by the linker MyD88 activates the transcription factor nuclear factor kappa B (NF-κB), thereby inducing gene expression of pro-inflammatory factors like tumor necrosis factor (TNF), IL-6, and IL-1β ( Foley, 2015 ). (frontiersin.org)
  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a pro-neurotoxicant that must be metabolized to 1-methyl-4-phenylpyridinium (MPP+) and taken up into striatal dopaminergic neurons to produce neurodegeneration. (cdc.gov)
  • In addition to preferentially damaging dopaminergic neurons, these agents share several common mechanisms of action including increasing neuronal oxidating stress, damaging mitochondrial complex I, and impairing the ubiquitin-proteasome system [3, 4]. (researchsquare.com)
  • MPP+ has affinity for the catecholamine uptake system, is taken up preferentially into dopaminergic neurons with cell bodies in the substantia nigra zona compacta, where it inhibits complex-1 of the electron transport chain. (avensonline.org)
  • Neuronal PC12 cells and ventral midbrain dopaminergic neurons were assessed in vitro for survival, transcription factor levels and Trib3 or Parkin expression after exposure to 6-hydroxydopamine or 1-methyl-4-phenylpyridinium with or without adaptaquin co-treatment. (puppyreading.com)
  • The present study examined whether crosstalk between cannabinoid (CB) and transient potential receptor vanilloid type 1 (TRPV1) could contribute to the survival of nigrostriatal dopamine neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD). (hindawi.com)
  • Many experimental studies demonstrated that TRPV1 activation by capsaicin (CAP) prevents the degeneration of nigrostriatal dopamine neurons in the 1-methyl-4-phenylpyridinium- (MPP + -) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) or 6-hydroxy dopamine (6-OHDA-) lesioned rodent model of PD via inhibiting glial-derived inflammatory responses and producing ciliary neurotrophic factor (CNTF) [ 11 - 13 ]. (hindawi.com)
  • Note: however that MPTP serves as a protoxin, via it metabolism by monoamine axidase B (MAO-B) to 1-methyl-4-phenylpyridinium (MPP+). (avensonline.org)
  • Treatment of SH-SY5Y cells with CBR-470-1, an inhibitor of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1), leads to methylglyoxal modification of Keap1, Keap1-Nrf2 disassociation, and increased expression of Nrf2 responsive genes. (aging-us.com)
  • Parkinson disease (PD) is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment. (medscape.com)
  • Parkinson disease is recognized as one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years. (medscape.com)
  • Niraparib is a potent and selective inhibitor of poly(ADP-ribose) polymerase (PARP) enzymes, PARP-1 and PARP-2. (drugbank.com)
  • 3,5-dibenzoyl-4-(3-phenoxyphenyl)-1,4-dihydro-2,6-dimethylpyridine (DP7): a new multidrug resistance inhibitor devoid of effects on Langendorff-perfused rat heart. (unisi.it)
  • This study was designed to assess the effect of hypoxia on AhR transcriptional KU-55933 DNA Damage/DNA Repair inhibitor responses after exposure to 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126). (mirnamimics.com)
  • 1 However, some cells can have defective or deficient HR resulting from specific mutations in DNA repair genes, such as BRCA1 and 2. (drugbank.com)
  • Although several genes have been implicated as monogenic causes of the disease, these genetic mutations are only responsible for approximately 10% of cases [1]. (researchsquare.com)
  • The remaining 90% of the cases are idiopathic, and different environmental exposures have been implicated as either protective factors (such as tobacco smoking and caffeine intake) or risk factors (such as heavy metals and pesticides exposure) [1]. (researchsquare.com)
  • 14 C-TEA uptake in hOCT1 plasmid DNA-transfected HeLa cells was trans -stimulated by unlabeled TEA and 1-methyl-4-phenyl-pyridinium. (aspetjournals.org)
  • 1991. Control of 1,2-dimethylhydrazine-induced crypt hyperplasia by naturalkiller cells and its relevance to carcinogenics. (cdc.gov)
  • Consistent with these findings, PGK1 depletion or knockout mimicked CBR-470-1-induced actions and rendered SH-SY5Y cells resistant to MPP + -induced cytotoxicity. (aging-us.com)
  • Collectively PGK1 inhibition by CBR-470-1 protects SH-SY5Y cells from MPP + via activation of the Keap1-Nrf2 cascade. (aging-us.com)
  • 4 If BER is impaired, SSBs accumulate and become DSBs, forcing cells to rely on other repair pathways, mainly the homologous recombination (HR) and the nonhomologous end joining, to repair DNA damages. (drugbank.com)
  • Uptake and superfusion experiments were performed on human embryonic kidney 293 cells permanently expressing the hSERT using [(3)H]serotonin (5-HT) and [(3)H]1-methyl-4-phenylpyridinium (MPP(+)) as substrates. (neurotransmitter.net)
  • The objective of this study was to define the relative contributions of alveolar overdistension and cyclic recruitment and "collapse" of Fer-1 manufacturer unstable lung units to membrane wounding of alveolar epithelial cells. (mirnamimics.com)
  • This results in extrapyramidal motor dysfunction, including tremor, rigidity, and bradykinesia [ 1 ] and decreased tyrosine hydroxylase (TH) and the production and storage of dopamine (DA) in the striatum [ 2,3 ]. (avensonline.org)
  • 3,5-Di-t-butyl-4-hydroxyanisole (DTBHA) activation of rat skeletal muscle sarcoplasmic reticulum Ca2+-ATPase. (unisi.it)
  • Mutations in ClC-1 are associated with myotonia congenita (MC) and result in loss of regulation of membrane excitability in skeletal muscle. (inforang.com)
  • 2,5-Di-t-butyl-1,4-benzohydroquinone (BHQ) inhibits vascular L-type Ca2+ channel via superoxide anion generation. (unisi.it)
  • 1987. The influence of physical activity in 1 ,2dimethylhydrazine induced colon carcinogenesis in the rat. (cdc.gov)
  • 6 Niraparib is selective towards PARP-1 and PARP-2. (drugbank.com)
  • Strain susceptibility and resistance to 1,2-dimethylhydrazine-induced enteric tumors in germfree rats (40146). (cdc.gov)
  • Parkinson's disease (PD) is a well-known neurodegenerative disorder that is characterized by the degeneration of dopamine neurons in the substantia nigra pars compacta (SNpc) and dopamine deficiency in the striatum (STR), consequently resulting in motor dysfunction [ 1 , 2 ]. (hindawi.com)
  • Parkinson's disease (PD) is the most common neurodegenerative movement disorder, estimated to affect 1% of the population over 65 years of age. (springer.com)
  • Re-evaluation of 1,2-dimethylhydrazine in the mouse bone marrow micronucleus assay: Observation of a positive response. (cdc.gov)
  • 4 If this strategy does not improve psychosis symptoms, physicians should consider use of cholinesterase inhibitors (eg, rivastigmine 6-12 mg/2-3 days, donepezil 5-10 mg daily, or galantamine 4-32 mg/2-3 days) or antipsychotic medication (clozapine 12.5-62.5 mg daily or quetiapine 12.5-75 mg daily). (neurologylive.com)
  • It is a chronic and progressive disease characterized predominantly by resting tremors, bradykinesia, muscular rigidity and postural instability, along with several non-motor symptoms [ 1 ]. (springer.com)
  • 4 Risperidone has also been shown to worsen motor function and thus is not recommended for PDP. (neurologylive.com)
  • Rosmarinic acid (RosA) is a water-soluble phenolic compound that is an ester of caffeic acid and 3, 4-dihydroxyphenyl lactic acid. (frontiersin.org)
  • In Part 1 of this report, we review data on the effects of estrogen (E), the anti-E tamoxifen (TMX), and testosterone (T) on methamphetamine (METH)-induced neurotoxicity in female and male CD-1 mice. (omeka.net)
  • 3,5-Dibenzoyl-4-(3-phenoxyphenyl)-1,4-dihydro-2,6-dimethylpyridine (DP7) as a new multidrug resistance reverting agent devoid of effects on vascular smooth muscle contractility. (unisi.it)
  • In addition, we found that the combined berberine and curcumin treatment had significant synergic effects on reducing soluble amyloid-β-peptide(1-42) production. (puppyreading.com)
  • In both culture and animal models, adaptaquin suppressed elevation of ATF4 and/or CHOP and induction of Trib3 in response to 1-methyl-4-phenylpyridinium and/or 6-hydroxydopamine. (puppyreading.com)
  • Antagonism by taurine on the ruthenium red-induced and 6-hydroxydopamine plus 1-methyl-4-phenylpyridinium-induced Ca2+ release from rat liver mitochondria. (unisi.it)
  • Concentrations and in vitro release of norepinephrine were determined from left and right olfactory bulbs of adult male CD-1 mice. (omeka.net)
  • 1988. Species-specific response to the rodent carcinogens 1,2-dimethylhydrazine and 1,2-dibromo-3-chloropropane in rodent bone-marrow micronucleus assays. (cdc.gov)
  • 1 PDP has been reported to affect up to 60% of patients over their lifetime, and this risk increases with age and larger doses of DA medications. (neurologylive.com)