| Name | tyrosine hydroxylase |
|---|---|
| Synonyms | Putative tyrosine hydroxylase variant; TH; TH protein; TYH; Truncated tyrosine hydroxylase; Tyrosine 3 hydroxylase; Tyrosine 3 monooxygenase; Tyrosine hydroxylase… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17047462 | Kim SJ, Kim JS, Cho HS, Lee HJ, Kim SY, Kim S, Lee SY, Chun HS: a component of rosemary (Rosmarinus officinalis L.) protects nigral dopaminergic neuronal cells. Neuroreport. 2006 Nov 6;17(16):1729-33. In this study, we investigated the protective effects of on rotenone-induced neurotoxicity in cultured dopaminergic cells. Furthermore, significantly increased the tyrosine hydroxylase, Nurr1, and extracellular signal-regulated kinase 1/2. |
1(0,0,0,1) | Details |
| 9449429 | Nakao N, Nakai K, Itakura T: Metabolic inhibition enhances selective toxicity of toward mesencephalic neurons in vitro. Brain Res. 1997 Nov 28;777(1-2):202-9. We investigated whether metabolic inhibition with rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, may enhance the toxicity of toward DA neurons in mesencephalic cultures. This was confirmed by cell survival estimation showing that tyrosine hydroxylase-positive DA cells are more vulnerable to the sequential exposure to the drugs than total cells. |
1(0,0,0,1) | Details |
| 19735655 | Quesada A, Micevych P, Handforth A: C-terminal mechano growth factor protects neurons: a novel peptide that induces heme oxygenase-1. Exp Neurol. 2009 Dec;220(2):255-66. Epub 2009 Sep 6. We show that a short 24-amino acid C-terminal peptide of MGF (MGF24) upregulates heme oxygenase-1 (HO-1) expression and protects SH-SY5Y cells against apoptosis and cell loss induced by three DA cell-specific neurotoxins: (6-OHDA), 1-methyl-4-phenylpyridinium (MPP (+)), and rotenone. In 6-OHDA-lesioned rats, central or peripheral MGF24 administration protects against the development of contralateral forelimb under-utilization, reduces ipsilateral nigral DA cell body loss, and attenuates tyrosine hydroxylase fiber loss in the ipsilateral striatum, independent of IGF-1 receptor activation. |
1(0,0,0,1) | Details |
| 19406215 | Nagel F, Bahr M, Dietz GP: Tyrosine hydroxylase-positive amacrine interneurons in the mouse retina are resistant against the application of various parkinsonian toxins. Brain Res Bull. 2009 Jun 30;79(5):303-9. Epub 2009 May 3. Toxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), (6-OHDA), or rotenone have been used to induce degeneration of dopaminergic (DA) neurons in the nigrostriatal pathway and to reproduce pathological characteristics of Parkinson's disease (PD). |
1(0,0,0,1) | Details |
| 12385818 | Alam M, Schmidt WJ: Rotenone destroys dopaminergic neurons and induces parkinsonian symptoms in rats. Behav Brain Res. 2002 Oct 17;136(1):317-24. This treatment caused depletion of in the posterior striatum (CPu) and prefrontal cortex and also reduced tyrosine hydroxylase-immunoreactivity in CPu. |
1(0,0,0,1) | Details |
| 17273802 | Luo C, Rajput AH, Akhtar S, Rajput A: Alpha-synuclein and tyrosine hydroxylase expression in acute rotenone toxicity. Int J Mol Med. 2007 Mar;19(3):517-21. In the substantia nigra of rotenone-treated rats, four of six had reduced numbers of tyrosine hydroxylase-positive neurons and all six had increased nigral alpha-synuclein expression. |
87(1,1,2,2) | Details |
| 15910763 | Grammatopoulos TN, Ahmadi F, Jones SM, Fariss MW, Weyhenmeyer JA, Zawada WM: Angiotensin II protects cultured midbrain dopaminergic neurons against rotenone-induced cell death. Brain Res. 2005 May 31;1045(1-2):64-71. Epub 2005 Apr 26. Acute exposure (20 h) to 20 nM rotenone reduced the number of tyrosine hydroxylase-positive (TH+) neurons by 50 +/- 6% when compared to untreated cultures. |
81(1,1,1,1) | Details |
| 12686372 | Sherer TB, Betarbet R, Kim JH, Greenamyre JT: Selective microglial activation in the rat rotenone model of Parkinson's disease. Neurosci Lett. 2003 May 1;341(2):87-90. In 50% of surviving rotenone-treated animals, there was nigrostriatal dopaminergic degeneration, marked by reduced tyrosine hydroxylase immunoreactivity). |
81(1,1,1,1) | Details |
| 17435593 | Lim ML, Mercer LD, Nagley P, Beart PM: Rotenone and MPP+ preferentially redistribute apoptosis-inducing factor in apoptotic neurons. Neuroreport. 2007 Mar 5;18(4):307-12. Tyrosine hydroxylase-positive neurons underwent apoptosis (shrinkage, less neurites) and 40% released apoptosis-inducing factor with rotenone (24 h), whereas cytochrome c release reached this value at 48 h when 70% of cells had released apoptosis-inducing factor-positive. 1-Methyl-4-phenylpyridinium produced similar redistribution patterns for both proteins. |
6(0,0,1,1) | Details |
| 17376993 | Mount MP, Lira A, Grimes D, Smith PD, Faucher S, Slack R, Anisman H, Hayley S, Park DS: Involvement of interferon-gamma in microglial-mediated loss of dopaminergic neurons. J Neurosci. 2007 Mar 21;27(12):3328-37. After this initial finding, we found that IFN-gamma-deficient mice displayed attenuated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced substantia nigra pars compacta dopaminergic cell loss along with reduced loss of striatal tyrosine hydroxylase and dopamine transporter fiber density. To examine more mechanistically the role of IFN-gamma in microglial activation, we evaluated the interactions between microglia and dopaminergic neurons in an in vitro mixed microglia/midbrain neuron rotenone-induced death paradigm. |
1(0,0,0,1) | Details |
| 19626387 | Monti B, Gatta V, Piretti F, Raffaelli SS, Virgili M, Contestabile A: is neuroprotective in the rotenone rat model of Parkinson's disease: involvement of alpha-synuclein. Neurotox Res. 2010 Feb;17(2):130-41. Epub 2009 Jul 21. The decrease of the dopaminergic marker tyrosine hydroxylase in substantia nigra and striatum caused by 7 days toxin administration was prevented in VPA-fed rats. |
1(0,0,0,1) | Details |
| 15790535 | Testa CM, Sherer TB, Greenamyre JT: Rotenone induces oxidative stress and dopaminergic neuron damage in organotypic substantia nigra cultures. Brain Res Mol Brain Res. 2005 Mar 24;134(1):109-18. Epub 2005 Jan 6. Chronic complex I inhibition over weeks by low dose (10-50 nM) rotenone in this system lead to dose- and time-dependent destruction of substantia nigra pars compacta neuron processes, morphologic changes, some neuronal loss, and decreased tyrosine hydroxylase (TH) protein levels. |
62(0,2,2,2) | Details |
| 17520785 | Yi PL, Tsai CH, Lu MK, Liu HJ, Chen YC, Chang FC: Interleukin-1beta mediates sleep alteration in rats with rotenone-induced parkinsonism. Sleep. 2007 Apr 1;30(4):413-25. This rotenone PD animal model successfully causes loss of tyrosine hydroxylase-immunopositive neurons in the substantia nigra; induces the events of sleep disturbance, such as excessive daytime sleepiness and insomnia during the nighttime, that are seen in patients with PD; and suppresses locomotion. |
32(0,1,1,2) | Details |
| 16343695 | Choi HJ, Lee SY, Cho Y, No H, Kim SW, Hwang O: causes mitochondrial dysfunction in dopaminergic cells: implications for Parkinson's disease. Neurochem Int. 2006 Mar;48(4):255-62. Epub 2005 Dec 15. We have previously suggested (BH4), an obligatory cofactor for the synthesis enzyme tyrosine hydroxylase and present selectively in monoaminergic neurons in the brain, as an endogenous molecule that contributes to the dopaminergic neurodegeneration. BH4 appears to be different from rotenone and MPP (+), the synthetic compounds used to generate Parkinson models, in its effect on complex IV. |
1(0,0,0,1) | Details |
| 17880941 | Rojo AI, Cavada C, de Sagarra MR, Cuadrado A: Chronic inhalation of rotenone or paraquat does not induce Parkinson's disease symptoms in mice or rats. Exp Neurol. 2007 Nov;208(1):120-6. Epub 2007 Aug 22. MPTP-treated mice developed motor deficits that correlated with a severe depletion of striatal levels, and loss of tyrosine hydroxylase staining in substantia nigra and striatum. |
1(0,0,0,1) | Details |
| 15890007 | Dukes AA, Korwek KM, Hastings TG: The effect of endogenous in rotenone-induced toxicity in PC12 cells. Antioxid Redox Signal. 2005 May-Jun;7(5-6):630-8. To determine whether endogenous DA makes PC12 cells more susceptible to rotenone, cells were treated with the tyrosine hydroxylase inhibitor alpha-methyl- (AMPT) to reduce DA levels prior to rotenone exposure, and then cell viability was measured. |
31(0,1,1,1) | Details |
| 20169778 | Radad K, Moldzio R, Rausch WD: Minocycline protects dopaminergic neurons against long-term rotenone toxicity. Can J Neurol Sci. 2010 Jan;37(1):81-5. RESULTS: Treatment of cultures with 5 and 20 nM of rotenone significantly decreased the survival of tyrosine hydroxylase immunoreactive neurons by 27 and 31% and increased the release of lactate dehydrogenase into the culture medium by 31 and 236%, respectively compared to untreated controls. |
19(0,0,3,4) | Details |
| 19442875 | Falk T, Zhang S, Sherman SJ: Pigment epithelium derived factor (PEDF) is neuroprotective in two in vitro models of Parkinson's disease. Neurosci Lett. 2009 Jul 17;458(2):49-52. Epub 2009 Apr 11. This was shown in (1) rotenone and (2) (6-OHDA) in vitro models. The cultures were fixed and analyzed after tyrosine hydroxylase (TH) immunocytochemical staining. |
1(0,0,0,1) | Details |
| 12358732 | Wu J, Chan P, Schroeder KM, Ellsworth K, Partridge LD: 1-Methyl-4-phenylpridinium (MPP+)-induced functional run-down of (A) receptor-mediated currents in acutely dissociated dopaminergic neurons. J Neurochem. 2002 Oct;83(1):87-99. The MPP+-induced I run-down can be prevented by a DA transporter inhibitor, mazindol, and can be mimicked by a metabolic inhibitor, rotenone. Corresponding to these patch-clamp data, tyrosine hydroxylase (TH) immunohistochemical staining showed that TH-positive cell loss was protected by PB during MPP+ perfusion. |
1(0,0,0,1) | Details |
| 16490285 | Saravanan KS, Sindhu KM, Senthilkumar KS, Mohanakumar KP: L-deprenyl protects against rotenone-induced, oxidative stress-mediated dopaminergic neurodegeneration in rats. Neurochem Int. 2006 Jul;49(1):28-40. Epub 2006 Feb 21. Unilateral stereotaxic intranigral infusion of rotenone caused significant decrease of striatal levels as measured employing HPLC-electrochemistry, and loss of tyrosine hydroxylase immunoreactivity in the perikarya of ipsilateral substantia nigra (SN) neurons and their terminals in the striatum. |
12(0,0,2,2) | Details |
| 16118017 | Huang J, Liu H, Gu W, Yan Z, Xu Z, Yang Y, Zhu X, Li Y: A delivery strategy for rotenone microspheres in an animal model of Parkinson's disease. Biomaterials. 2006 Feb;27(6):937-46. Epub 2005 Aug 22. The rotenone microspheres (9 mg/kg) produced typical PD symptoms in rats, for example, the cataleptic behavior test demonstrated a obviously prolonged descent latency compared with control animals after administration, and the tyrosine hydroxylase (TH) immunohistochemistry tests showed typical histological evidence of selective degeneration of the nigrostriatal dopaminergic system (striatum and substantia nigra) in rotenone microspheres-treated rats. |
6(0,0,1,1) | Details |
| 12504867 | Bywood PT, Johnson SM: Mitochondrial complex inhibitors preferentially damage substantia nigra neurons in rat brain slices. Exp Neurol. 2003 Jan;179(1):47-59. Brain slices (400 microm) were incubated at 35 degrees C for 2 h in the presence or absence of mitochondrial complex inhibitors, rotenone, MPP+, 3-nitropropionic acid, and antimycin A. The slices were then fixed, recut into 30-microm sections, and immunolabeled for tyrosine hydroxylase (TH) to identify catecholamine neurons and to quantify loss of TH-labeled dendrites after treatment. |
1(0,0,0,1) | Details |
| 15996475 | Kress GJ, Reynolds IJ: Dopaminergic neurotoxins require excitotoxic stimulation in organotypic cultures. Neurobiol Dis. 2005 Dec;20(3):639-45. Epub 2005 Jun 29. We have investigated the properties of the dopaminergic neurotoxins 1-methyl-4-phenylpyridinium and rotenone using an organotypic culture that included slices of substantia nigra, striatum and cortex maintained for about 20 days in vitro. At this age, the organotypic culture contains dopaminergic neurons, visualized using tyrosine hydroxylase (TH) immunohistochemistry, that project into the striatal slice and extend up to 1 mm into the cortical slice. |
1(0,0,0,1) | Details |
| 17439496 | Vehovszky A, Szabo H, Hiripi L, Elliott CJ, Hernadi L: Behavioural and neural deficits induced by rotenone in the pond snail Lymnaea stagnalis. Eur J Neurosci. 2007 Apr;25(7):2123-30. Immunostaining revealed that the tyrosine hydroxylase immunoreactivity decreased below the detectable level in both the RPeD1 cell body and its axonal processes. |
1(0,0,0,1) | Details |
| 15925285 | Milusheva E, Baranyi M, Kittel A, Sperlagh B, Vizi ES: Increased sensitivity of striatal release to H2O2 upon chronic rotenone treatment. Free Radic Biol Med. 2005 Jul 1;39(1):133-42. Epub 2005 Mar 25. The content in the rat striatum is decreased simultaneously with the progressive loss of tyrosine hydroxylase (TH) immunoreactivity in response to chronic intravenous rotenone infusion. |
6(0,0,1,1) | Details |
| 14622122 | Ahmadi FA, Linseman DA, Grammatopoulos TN, Jones SM, Bouchard RJ, Freed CR, Heidenreich KA, Zawada WM: The pesticide rotenone induces caspase-3-mediated apoptosis in ventral mesencephalic dopaminergic neurons. J Neurochem. 2003 Nov;87(4):914-21. After 11 h of exposure to 30 nm rotenone, the number of neurons identified by tyrosine hydroxylase (TH) immunostaining declined rapidly with only 23% of the neurons surviving. |
6(0,0,1,1) | Details |
| 18197244 | Marella M, Seo BB, Nakamaru-Ogiso E, Greenamyre JT, Matsuno-Yagi A, Yagi T: Protection by the NDI1 gene against neurodegeneration in a rotenone rat model of Parkinson's disease. PLoS One. 2008 Jan 16;3(1):e1433. It was clear that the introduction of the Ndi1 protein in the substantia nigra rendered resistance to the deleterious effects caused by rotenone exposure as assessed by the levels of tyrosine hydroxylase and |
6(0,0,1,1) | Details |
| 15530876 | Ling Z, Chang QA, Tong CW, Leurgans SE, Lipton JW, Carvey PM: Rotenone potentiates neuron loss in animals exposed to lipopolysaccharide prenatally. Exp Neurol. 2004 Dec;190(2):373-83. Tyrosine hydroxylase-immunoreactive (THir) cell counts were used as an index of DA neuron survival. |
1(0,0,0,1) | Details |
| 20041858 | Hu LF, Lu M, Tiong CX, Dawe GS, Hu G, Bian JS: Neuroprotective effects of on Parkinson's disease rat models. Aging Cell. 2009 Dec 23. Systemic administration of NaHS (an H (2) S donor) dramatically reversed the progression of movement dysfunction, loss of tyrosine-hydroxylase positive neurons in the SN and the elevated malondialdehyde level in injured striatum in the 6-OHDA-induced PD model. Similarly, administration of NaHS also prevented the development of PD induced by rotenone. |
1(0,0,0,1) | Details |
| 14766796 | Lapointe N, St-Hilaire M, Martinoli MG, Blanchet J, Gould P, Rouillard C, Cicchetti F: Rotenone induces non-specific central nervous system and systemic toxicity. FASEB J. 2004 Apr;18(6):717-9. Epub 2004 Feb 6. |
0(0,0,0,0) | Details |
| 19924288 | Xiong N, Huang J, Zhang Z, Zhang Z, Xiong J, Liu X, Jia M, Wang F, Chen C, Cao X, Liang Z, Sun S, Lin Z, Wang T: Stereotaxical infusion of rotenone: a reliable rodent model for Parkinson's disease. PLoS One. 2009 Nov 18;4(11):e7878. Four weeks after ST rotenone administration, tyrosine hydroxylase (TH) immunoreactivity in the infusion side decreased by 43.7%, in contrast to a 75.8% decrease observed in rats treated systemically with rotenone (SYS). |
6(0,0,1,1) | Details |
| 16624952 | Jiang Q, Yan Z, Feng J: Activation of group III metabotropic glutamate receptors attenuates rotenone toxicity on dopaminergic neurons through a microtubule-dependent mechanism. J Neurosci. 2006 Apr 19;26(16):4318-28. Our previous study has shown that the microtubule-depolymerizing activity of rotenone plays a critical role in its selective toxicity on tyrosine hydroxylase-positive (TH+) neurons in rat embryonic midbrain neuronal cultures. |
6(0,0,1,1) | Details |
| 12950443 | He Y, Imam SZ, Dong Z, Jankovic J, Ali SF, Appel SH, Le W: Role of in rotenone-induced nigro-striatal injury. J Neurochem. 2003 Sep;86(6):1338-45. After administration of rotenone in rats for 40 days, there was a moderate but significant injury of the nigro-striatal pathway indicated by a 47% decrease in striatal levels and a 28% loss of substantia nigra tyrosine hydroxylase-immunopositive neurons. |
6(0,0,1,1) | Details |
| 16488175 | Phinney AL, Andringa G, Bol JG, Wolters ECh, van Muiswinkel FL, van Dam AM, Drukarch B: Enhanced sensitivity of dopaminergic neurons to rotenone-induced toxicity with aging. Parkinsonism Relat Disord. 2006 May;12(4):228-38. Epub 2006 Feb 20. |
0(0,0,0,0) | Details |
| 15635186 | Fujikawa T, Kanada N, Shimada A, Ogata M, Suzuki I, Hayashi I, Nakashima K: Effect of sesamin in Acanthopanax senticosus HARMS on behavioral dysfunction in rotenone-induced parkinsonian rats. Biol Pharm Bull. 2005 Jan;28(1):169-72. We also examined how sesamin affected the rotenone-induced loss of tyrosine hydroxylase (TH) or glial cell line-derived neurotrophic factor (GDNF)-positive neurons in the midbrain of rats. |
6(0,0,1,1) | Details |
| 15144868 | Fleming SM, Zhu C, Fernagut PO, Mehta A, DiCarlo CD, Seaman RL, Chesselet MF: Behavioral and immunohistochemical effects of chronic intravenous and subcutaneous infusions of varying doses of rotenone. Exp Neurol. 2004 Jun;187(2):418-29. To address this question, vehicle or rotenone (2.0, 2.5, or 3.5 mg/kg/day) was administered intravenously or subcutaneously for 21 days to adult rats, and rotenone effects on survival, motor behavior, and striatal tyrosine hydroxylase immunoreactivity (TH-IR) were examined. |
6(0,0,1,1) | Details |
| 19644772 | Aoki E, Yokoyama H, Kimoto H, Yano R, Kato H, Araki T: Chronic administration with rotenone does not enhance MPTP neurotoxicity in C57BL/6 mice. J Mol Neurosci. 2010 May;41(1):17-24. Epub 2009 Jul 31. Our Western blot analysis study demonstrated that the change of tyrosine hydroxylase and glial fibrillary acidic protein protein levels in MPTP-treated mice was similar than that in MPTP + rotenone-treated animals. |
6(0,0,1,1) | Details |
| 10486562 | Hohler B, Lange B, Holzapfel B, Goldenberg A, Hanze J, Sell A, Testan H, Moller W, Kummer W: Hypoxic upregulation of tyrosine hydroxylase gene expression is paralleled, but not induced, by increased generation of reactive species in PC12 cells. FEBS Lett. 1999 Aug 20;457(1):53-6. This increase is abolished by intracellular scavenging by Mn (III)-tetrakis (1-methyl-4-pyridyl)- and reduced or absent in the presence of the flavoprotein/complex I inhibitors, diphenyl-eneiodonium and rotenone. |
0(0,0,0,0) | Details |
| 16006012 | Nieto M, Gil-Bea FJ, Dalfo E, Cuadrado M, Cabodevilla F, Sanchez B, Catena S, Sesma T, Ribe E, Ferrer I, Ramirez MJ, Gomez-Isla T: Increased sensitivity to MPTP in human alpha-synuclein A30P transgenic mice. Neurobiol Aging. 2006 Jun;27(6):848-56. Epub 2005 Jul 11. We investigated the possible interaction between genetic factors and neurotoxins by testing whether alpha-synuclein A30P Tg5093 transgenic mice show increased sensitivity to secondary toxic insults like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone. |
0(0,0,0,0) | Details |
| 19385059 | Cannon JR, Tapias V, Na HM, Honick AS, Drolet RE, Greenamyre JT: A highly reproducible rotenone model of Parkinson's disease. Neurobiol Dis. 2009 May;34(2):279-90. Rotenone treatment caused a 45% loss of tyrosine hydroxylase-positive substantia nigra neurons and a commensurate loss of striatal |
6(0,0,1,1) | Details |
| 18155613 | Ravenstijn PG, Merlini M, Hameetman M, Murray TK, Ward MA, Lewis H, Ball G, Mottart C, de Ville de Goyet C, Lemarchand T, van Belle K, O'Neill MJ, Danhof M, de Lange EC: The exploration of rotenone as a toxin for inducing Parkinson's disease in rats, for application in BBB transport and PK-PD experiments. J Pharmacol Toxicol Methods. 2008 Mar-Apr;57(2):114-30. Epub 2007 Nov 13. At different times following rotenone infusion, behaviour, histopathology (tyrosine hydroxylase and alpha-synuclein immunocytochemistry), peripheral organ pathology (adrenals, heart, kidney, liver, lung, spleen and stomach) were assessed. |
6(0,0,1,1) | Details |
| 15694918 | Kotake Y, Taguchi R, Okuda K, Sekiya Y, Tasaki Y, Hirobe M, Ohta S: Neuroprotective effect of 1-methyl-1,2,3,4-tetrahydroisoquinoline on cultured rat mesencephalic neurons in the presence or absence of various neurotoxins. Brain Res. 2005 Feb 8;1033(2):143-50. In this study, we examined the neuroprotective effect of 1MeTIQ against four dopaminergic neurotoxins, 1-methyl-4-phenylpyridinuim ion, rotenone, and l-benzyl-1,2,3,4-tetrahydroisoquinoline, in cultured rat mesencephalic neurons. 1MeTIQ exerted neuroprotective action against all these toxins. |
0(0,0,0,0) | Details |
| 15384065 | Zhu C, Vourc'h P, Fernagut PO, Fleming SM, Lacan S, Dicarlo CD, Seaman RL, Chesselet MF: Variable effects of chronic subcutaneous administration of rotenone on striatal histology. J Comp Neurol. 2004 Oct 25;478(4):418-26. |
0(0,0,0,0) | Details |
| 16725203 | Kou J, Klorig DC, Bloomquist JR: Potentiating effect of the ATP-sensitive potassium channel blocker glibenclamide on complex I inhibitor neurotoxicity in vitro and in vivo. Neurotoxicology. 2006 Sep;27(5):826-34. Epub 2006 Apr 28. We measured the ability of mitochondrial inhibitors of complexes I (rotenone, MPP (+), and HPP (+)), II (amdro), IV (Na and an uncoupler (dinoseb) to release preloaded from murine striatal synaptosomes. |
0(0,0,0,0) | Details |
| 15540952 | Caboni P, Sherer TB, Zhang N, Taylor G, Na HM, Greenamyre JT, Casida JE: Rotenone, deguelin, their metabolites, and the rat model of Parkinson's disease. Chem Res Toxicol. 2004 Nov;17(11):1540-8. |
0(0,0,0,0) | Details |
| 16573651 | Casarejos MJ, Menendez J, Solano RM, Rodriguez-Navarro JA, Garcia de Yebenes J, Mena MA: Susceptibility to rotenone is increased in neurons from parkin null mice and is reduced by minocycline. J Neurochem. 2006 May;97(4):934-46. Epub 2006 Mar 29. ROT (0.025-0.1 microm) produced a dose-dependent selective reduction of tyrosine hydroxylase-immunoreactive cells and of other neurons, as shown by the immunoreactivity to microtubule-associated protein 2 in PK-KO cultures, suggesting that the toxic effect of ROT involved and other types of neurons. |
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| 16543240 | Seo BB, Nakamaru-Ogiso E, Flotte TR, Matsuno-Yagi A, Yagi T: In vivo complementation of complex I by the yeast Ndi1 enzyme. J Biol Chem. 2006 May 19;281(20):14250-5. Epub 2006 Mar 16. We have shown previously that the single subunit rotenone-insensitive -quinone oxidoreductase (Ndi1) of Saccharomyces cerevisiae mitochondria can restore oxidation in complex I-deficient mammalian cells. The degree of neurodegeneration in the nigrostriatal system was assessed immunohistochemically through the analysis of tyrosine hydroxylase and glial fibrillary acidic protein. |
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| 17923380 | Radad K, Gille G, Rausch WD: Dopaminergic neurons are preferentially sensitive to long-term rotenone toxicity in primary cell culture. Toxicol In Vitro. 2008 Feb;22(1):68-74. Epub 2007 Sep 1. The number of tyrosine hydroxylase immunoreactive (TH (+)) neurons and total hematoxylin-stained nuclei were counted. |
1(0,0,0,1) | Details |
| 17900761 | Larsen TR, Soderling AS, Caidahl K, Roepstorff P, Gramsbergen JB: Nitration of soluble proteins in organotypic culture models of Parkinson's disease. Neurochem Int. 2008 Feb;52(3):487-94. Epub 2007 Aug 19. Here we quantified protein-bound (3-NT) by a novel gas chromatography/negative chemical ionization tandem mass spectrometry technique and DA and by HPLC in tissues or medium of organotypic, mouse mesencephalon cultures after acute or chronic treatments with the donor 3-morpholino-sydnonimine (SIN-1), the dopaminergic toxin 1-methyl-4-phenylpyridinium (MPP (+)) or the lipophilic complex I inhibitor rotenone. |
0(0,0,0,0) | Details |
| 10514095 | Duan W, Zhang Z, Gash DM, Mattson MP: Participation of prostate apoptosis response-4 in degeneration of dopaminergic neurons in models of Parkinson's disease. Ann Neurol. 1999 Oct;46(4):587-97. The increase in Par-4 levels occurs in both neuronal cell bodies in the substantia nigra and their axon terminals in the striatum, and precedes loss of tyrosine hydroxylase immunoreactivity and cell death. Exposure of cultured human dopaminergic neural cells to the complex I inhibitor rotenone, or to Fe2+, resulted in Par-4 induction, mitochondrial dysfunction, and subsequent apoptosis. |
1(0,0,0,1) | Details |
| 14663204 | Sakka N, Sawada H, Izumi Y, Kume T, Katsuki H, Kaneko S, Shimohama S, Akaike A: is involved in selectivity of dopaminergic neuronal death by rotenone. Neuroreport. 2003 Dec 19;14(18):2425-8. The toxicity was significantly prevented by a membrane-permeable superoxide dismutase mimetic and alpha-methyl- (alpha-MT), a tyrosine hydroxylase inhibitor. |
1(0,0,0,1) | Details |
| 15627486 | Mercer LD, Kelly BL, Horne MK, Beart PM: Dietary polyphenols protect neurons from oxidative insults and apoptosis: investigations in primary rat mesencephalic cultures. Biochem Pharmacol. 2005 Jan 15;69(2):339-45. Epub 2004 Nov 23. Primary mesencephalic cultures were sensitive to oxidative insults peroxide, rotenone, and N-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium hydrochloride (MPP+)) which produced concentration-dependent decreases in cellular viability across an apoptotic-necrotic continuum of injury. Flavonoids chrysin, puerarin, genestein) protected mesencephalic cultures from injury by MPP+, which was shown by DNA fragmentation studies and tyrosine hydroxylase (TH) immunocytochemistry of DA neurones to occur by apoptosis. |
1(0,0,0,1) | Details |
| 17555550 | Hirata Y, Kiuchi K: Rapid down-regulation of Ret following exposure of dopaminergic neurons to neurotoxins. J Neurochem. 2007 Sep;102(5):1606-13. Epub 2007 Jun 7. Treatment of mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine caused decreases in levels of Ret, a tyrosine kinase receptor for glial cell line-derived neurotrophic factor (GDNF) in the striatum, under the condition in which tyrosine hydroxylase was moderately decreased and the GDNF family receptor alpha1, another receptor of GDNF that is the ligand-binding subunit, were unaffected. Down-regulation of Ret was also observed in -producing PC12 cells undergoing apoptosis induced by rotenone, another toxic substance for dopaminergic neurons, while other cellular components were not affected. |
1(0,0,0,1) | Details |
| 18036194 | Milusheva E, Baranyi M, Kittel A, Fekete A, Zelles T, Vizi ES, Sperlagh B: Modulation of dopaminergic neurotransmission in rat striatum upon in vitro and in vivo diclofenac treatment. J Neurochem. 2008 Apr;105(2):360-8. Epub 2007 Nov 25. In conclusion, whereas in vitro DCF pre-treatment resembles the effect of the mitochondrial toxin rotenone, in vivo it rather counteracts than aggravates dopaminergic dysfunction. The intensity of tyrosine hydroxylase immunoreactivity in the striatum was highly variable, and both decrease and increase were observed in individual rats. |
1(0,0,0,1) | Details |
| 18579341 | Sai Y, Wu Q, Le W, Ye F, Li Y, Dong Z: Rotenone-induced PC12 cell toxicity is caused by oxidative stress resulting from altered metabolism. Toxicol In Vitro. 2008 Sep;22(6):1461-8. Epub 2008 May 4. Tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT (2)) were markedly down-regulated, and dopamine transporter (DAT) was up-regulated in the cells. |
1(0,0,0,1) | Details |
| 15240412 | Gille G, Hung ST, Reichmann H, Rausch WD: Oxidative stress to dopaminergic neurons as models of Parkinson's disease. Ann N Y Acad Sci. 2004 Jun;1018:533-40. The effects of exogenous toxins (MPP (+), rotenone) and potentially properties of on the survival rate of dopaminergic neurons in dissociated primary culture are presented. Moreover, a preserving potential of the antioxidant and bioenergetic (10) (10)) on the activities of tyrosine hydroxylase (TH), complexes I and II of the respiratory chain, and hexokinase activity in striatal slice cultures against MPP (+) is demonstrated. |
1(0,0,0,1) | Details |
| 17690729 | Feng Y, Liang ZH, Wang T, Qiao X, Liu HJ, Sun SG: alpha-Synuclein redistributed and aggregated in rotenone-induced Parkinson's disease rats. Neurosci Bull. 2006 Sep;22(5):288-93. The expression of tyrosine hydroxylase (TH) or ASN protein was determined by anti-TH or anti-alpha-synuclein immunohistochemistry, respectively. |
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| 16085056 | Bae SY, Xu Q, Hutchinson D, Colton CA: Y+ and y+ transporters in neuronal cells expressing tyrosine hydroxylase. Biochim Biophys Acta. 2005 Aug 15;1745(1):65-73. Epub 2005 Feb 9. Short term exposure to the oxidizing agents, rotenone and Angeli's salt, but not FeSO4, increases transport. |
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| 11205140 | Waldmeier PC, Boulton AA, Cools AR, Kato AC, Tatton WG: Neurorescuing effects of the GAPDH ligand CGP 3466B. J Neural Transm Suppl. 2000;(60):197-214. It also partially prevented the loss of tyrosine hydroxylase immunoreactivity in the substantia nigra of 6-OHDA-lesioned rats and improved motor function in these animals. In concentrations ranging from 10 (-13)-10 (-5) M, it rescues partially differentiated PC12 cells from apoptosis induced by trophic withdrawal, cerebellar granule cells from apoptosis induced by cytosine arabinoside, rat embryonic mesencephalic dopaminergic cells from death caused by MPP+, and PAJU human neuroblastoma cells from death caused by rotenone. |
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| 18289173 | Lin CH, Huang JY, Ching CH, Chuang JI: reduces the neuronal loss, downregulation of dopamine transporter, and upregulation of D2 receptor in rotenone-induced parkinsonian rats. J Pineal Res. 2008 Mar;44(2):205-13. Rotenone subcutaneously infused for 14 days induced PD symptoms in rats, as indicated by reduced spontaneous locomotor activity (hypokinesis), loss of tyrosine hydroxylase (TH, a marker enzyme for neurons) immunoreactivity in the substantia nigra and striatum, obvious alpha-synuclein accumulation, downregulated DAT protein expression, and upregulated D2R expression. |
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| 19653878 | Barber-Singh J, Seo BB, Nakamaru-Ogiso E, Lau YS, Matsuno-Yagi A, Yagi T: Neuroprotective effect of long-term NDI1 gene expression in a chronic mouse model of Parkinson disorder. Rejuvenation Res. 2009 Aug;12(4):259-67. Previously, we showed that the internal rotenone-insensitive -quinone oxidoreductase (NDI1) gene from Saccharomyces cerevisiae (baker's yeast) can be successfully inserted into the mitochondria of mice and rats and the expressed enzyme was found to be fully functional. We showed that expression of Ndi1 was able to significantly prevent the loss of and tyrosine hydroxylase as well as the dopaminergic transporters in the striatum of the chronic Parkinsonian mice. |
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| 15936733 | Saravanan KS, Sindhu KM, Mohanakumar KP: Acute intranigral infusion of rotenone in rats causes progressive biochemical lesions in the striatum similar to Parkinson's disease. Brain Res. 2005 Jul 12;1049(2):147-55. A significant decrease in tyrosine hydroxylase immunoreactivity in the striatum (73 +/- 8.4% as assessed by densitometric studies) or in SN ipsilateral to the side of infusion suggested nigrostriatal neuronal degeneration. |
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