Monoamine neurotoxin

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Oxidopamine (6-hydroxydopamine), a selective dopaminergic and noradrenergic neurotoxin. 6-Hydroxydopamine.svg
Oxidopamine (6-hydroxydopamine), a selective dopaminergic and noradrenergic neurotoxin.

A monoamine neurotoxin, or monoaminergic neurotoxin, is a drug that selectively damages or destroys monoaminergic neurons. [1] Monoaminergic neurons are neurons that signal via stimulation by monoamine neurotransmitters including serotonin, dopamine, and norepinephrine. [1]

Contents

Examples of monoamine neurotoxins include the serotonergic neurotoxins para-chloroamphetamine (PCA), methylenedioxymethamphetamine (MDMA), and 5,7-dihydroxytryptamine (5,7-DHT); [2] the dopaminergic neurotoxins oxidopamine (6-hydroxydopamine), MPTP, and methamphetamine; and the noradrenergic neurotoxins oxidopamine and DSP-4. [1]

In the case of serotonergic neurotoxins like MDMA, research suggests that simultaneous induction of serotonin and dopamine release, serotonin depletion, dopamine uptake and metabolism, hyperthermia, oxidative stress and antioxidant depletion, and/or drug metabolites may all be involved in the neurotoxicity. [3] [4] On the other hand, there is evidence that drug metabolites may not be involved. [3] [4]

Dopaminergic neurotoxins can induce a Parkinson's disease-like condition in animals and humans. [1] [5] Serotonergic neurotoxins have been associated with cognitive and memory deficits and psychiatric changes. [6] [7] [8] [9]

List of monoamine neurotoxins

Serotonergic neurotoxins

Phenethylamines

Tryptamines

2-Aminoindans

Dopaminergic neurotoxins

Phenethylamines

Dopamine and metabolites

Tryptamines

Pesticides

Others

Noradrenergic neurotoxins

Unsorted or unknown

See also

Related Research Articles

<span class="mw-page-title-main">Empathogen</span> Class of psychoactive drugs that produce empathic experiences

Empathogens or entactogens are a class of psychoactive drugs that induce the production of experiences of emotional communion, oneness, relatedness, emotional openness—that is, empathy or sympathy—as particularly observed and reported for experiences with 3,4-methylenedioxymethamphetamine (MDMA). This class of drug is distinguished from the classes of hallucinogen or psychedelic, and amphetamine or stimulants. Major members of this class include MDMA, MDA, MDEA, MDOH, MBDB, 5-APB, 5-MAPB, 6-APB, 6-MAPB, methylone, mephedrone, GHB, αMT, and αET, MDAI among others. Most entactogens are phenethylamines and amphetamines, although several, such as αMT and αET, are tryptamines. When referring to MDMA and its counterparts, the term MDxx is often used. Entactogens are sometimes incorrectly referred to as hallucinogens or stimulants, although many entactogens such as ecstasy exhibit psychedelic or stimulant properties as well.

<span class="mw-page-title-main">MPTP</span> Chemical compound

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is an organic compound. It is classified as a tetrahydropyridine. It is of interest as a precursor to the monoaminergic neurotoxin MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. It has been used to study disease models in various animals.

<span class="mw-page-title-main">Oxidopamine</span> Chemical compound

Oxidopamine, also known as 6-hydroxydopamine (6-OHDA) or 2,4,5-trihydroxyphenethylamine, is a synthetic monoaminergic neurotoxin used by researchers to selectively destroy dopaminergic and noradrenergic neurons in the brain.

<span class="mw-page-title-main">5,7-Dihydroxytryptamine</span> Chemical compound

5,7-Dihydroxytryptamine (5,7-DHT) is a monoaminergic neurotoxin used in scientific research to decrease concentrations of serotonin in the brain. The mechanism behind this effect is not well understood, but it is speculated to selectively destroy serotonergic neurons, in a manner similar to the dopaminergic neurotoxicity of 6-hydroxydopamine (6-OHDA). What is known is that this compound is in fact not selective in depleting serotonin content, but also depletes norepinephrine. To selectively deplete serotonin stores, it is commonly administered in conjunction with desmethylimipramine (desipramine), which inhibits the norepinephrine transporter.

<i>para</i>-Chloroamphetamine Chemical compound

para-Chloroamphetamine (PCA), also known as 4-chloroamphetamine (4-CA), is a serotonin–norepinephrine–dopamine releasing agent (SNDRA) and serotonergic neurotoxin of the amphetamine family. It is used in scientific research in the study of the serotonin system, as a serotonin releasing agent (SRA) at lower doses to produce serotonergic effects, and as a serotonergic neurotoxin at higher doses to produce long-lasting depletions of serotonin.

<span class="mw-page-title-main">MDAI</span> Chemical compound

MDAI, also known as 5,6-methylenedioxy-2-aminoindane, is an entactogen drug of the 2-aminoindane group which is related to MDMA and produces similar subjective effects.

<span class="mw-page-title-main">Monoamine releasing agent</span> Class of compounds

A monoamine releasing agent (MRA), or simply monoamine releaser, is a drug that induces the release of one or more monoamine neurotransmitters from the presynaptic neuron into the synapse, leading to an increase in the extracellular concentrations of the neurotransmitters and hence enhanced signaling by those neurotransmitters. The monoamine neurotransmitters include serotonin, norepinephrine, and dopamine; monoamine releasing agents can induce the release of one or more of these neurotransmitters.

<span class="mw-page-title-main">Serotonin releasing agent</span> Class of compounds

A serotonin releasing agent (SRA) is a type of drug that induces the release of serotonin into the neuronal synaptic cleft. A selective serotonin releasing agent (SSRA) is an SRA with less significant or no efficacy in producing neurotransmitter efflux at other types of monoamine neurons, including dopamine and norepinephrine neurons.

α-Methyldopamine Chemical compound

α-Methyldopamine (α-Me-DA), also known as 3,4-dihydroxyamphetamine or as catecholamphetamine, is a research chemical of the catecholamine and amphetamine families. It is a monoamine releasing agent and a metabolite of MDMA and MDA. The bis-glutathionyl metabolite of α-methyldopamine is slightly neurotoxic when directly injected into the brain's ventricles.

<span class="mw-page-title-main">UWA-101</span> Chemical compound

UWA-101 is a phenethylamine derivative researched as a potential treatment for Parkinson's disease. Its chemical structure is very similar to that of the illegal drug MDMA, the only difference being the replacement of the α-methyl group with an α-cyclopropyl group. MDMA has been found in animal studies and reported in unauthorised human self-experiments to be effective in the short-term relief of side-effects of Parkinson's disease therapy, most notably levodopa-induced dyskinesia. However the illegal status of MDMA and concerns about its potential for recreational use, neurotoxicity and potentially dangerous side effects mean that it is unlikely to be investigated for medical use in this application, and so alternative analogues were investigated.

<span class="mw-page-title-main">5-MAPB</span> Chemical compound

5-MAPB, also known as 5-(N-methyl-2-aminopropyl)benzofuran, is an entactogen and designer drug of the amphetamine family that is similar to MDMA in its structure and effects.

<span class="mw-page-title-main">2,4,5-Trihydroxymethamphetamine</span> Chemical compound

2,4,5-Trihydroxymethamphetamine is a neurotoxin and a metabolite of MDMA. It has structural similarity to the dopamine neurotoxin 6-hydroxydopamine, and produces lasting serotonin deficits when administered centrally.

<span class="mw-page-title-main">Animal models of Parkinson's disease</span> Models used in Parkinsons disease research

Animal models of Parkinson's disease are essential in the research field and widely used to study Parkinson's disease. Parkinson's disease is a neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of the dopamine neurons in the brain, results in motor dysfunction, ultimately causing the four cardinal symptoms of PD: tremor, rigidity, postural instability, and bradykinesia. It is the second most prevalent neurodegenerative disease, following Alzheimer's disease. It is estimated that nearly one million people could be living with PD in the United States.

<span class="mw-page-title-main">5,6-Dihydroxytryptamine</span> A selective serotonergic neurotoxin used in scientific research

5,6-Dihydroxytryptamine (5,6-DHT) is a monoaminergic neurotoxin and tryptamine derivative related to serotonin (5-hydroxytryptamine) and 5,7-dihydroxytryptamine (5,7-DHT). It is a relatively selective serotonergic neurotoxin, but also acts as a dopaminergic and noradrenergic neurotoxin at higher doses. In addition, it produces widespread generalized toxicity at higher doses. Its selective serotonergic neurotoxicity is due to its high affinity for the serotonin transporter (SERT). Because of its SERT affinity, 5,6-DHT has activity as a serotonin reuptake inhibitor.

<span class="mw-page-title-main">ODMA (drug)</span> MDMA analogue

ODMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzoxadiazole ring. TDMA and SeDMA are closely related analogues. ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024.

<span class="mw-page-title-main">TDMA (drug)</span> MDMA analogue

TDMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzothiadiazole ring. ODMA and SeDMA are closely related analogues. ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024.

<span class="mw-page-title-main">SeDMA</span> MDMA analogue

SeDMA is a bioisosteric analogue of 3,4-methylenedioxy-N-methylamphetamine (MDMA) which was developed in an attempt to create an improved MDMA alternative for potential clinical use. It is the analogue of MDMA in which the 1,3-benzodioxole ring has been replaced with a 2,1,3-benzoselenadiazole ring. ODMA and TDMA are closely related analogues. ODMA, TDMA, and SeDMA are releasing agents of serotonin, norepinephrine, and dopamine similarly to MDMA. However, they are less potent and efficacious in activating the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors than MDMA and show differing and potentially improved metabolic and pharmacokinetic properties in comparison. ODMA, TDMA, and SeDMA were first described in the scientific literature in June 2024.

<span class="mw-page-title-main">3,4-Dihydroxymethamphetamine</span> MDMA metabolite

3,4-Dihydroxymethamphetamine, or 3,4-dihydroxy-N-methylamphetamine, also known as α-methylepinine or α,N-dimethyldopamine, is the major metabolite of 3,4-methylenedioxy-N-methylamphetamine (MDMA). It is formed from MDMA by O-demethylation via cytochrome P450 enzymes including CYP2D6 as well as CYP1A2 and CYP3A4. Like MDMA, HHMA is a monoamine releasing agent.

2′-NH<sub>2</sub>-MPTP Monoaminergic neurotoxin

2′-NH2-MPTP, also known as 2′-amino-MPTP, is a monoaminergic neurotoxin that was derived from MPTP and is used in scientific research to lesion brain monoaminergic systems in animals. Whereas MPTP is a selective dopaminergic neurotoxin, 2′-NH2-MPTP is a specific serotonergic and noradrenergic neurotoxin that does not affect dopaminergic neurons. 2′-NH2-MPTP is transported by the serotonin transporter (SERT) into serotonergic neurons and by the norepinephrine transporter (NET) into noradrenergic neurons, and its serotonergic and noradrenergic neurotoxicity is dependent on this transport by the SERT and NET, respectively. 2′-NH2-MPTP was first described in the scientific literature by 1993.

<span class="mw-page-title-main">Borax combo</span> Designer drug combination mimicking MDMA

The Borax combo, also known by the informal brand names Blue Bliss and Pink Star, is a combination recreational and designer drug described as an MDMA-like entactogen.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 Kostrzewa RM (2022). "Survey of Selective Monoaminergic Neurotoxins Targeting Dopaminergic, Noradrenergic, and Serotoninergic Neurons". Handbook of Neurotoxicity. Cham: Springer International Publishing. pp. 159–198. doi:10.1007/978-3-031-15080-7_53. ISBN   978-3-031-15079-1.
  2. 1 2 3 4 5 6 7 8 Baumgarten HG, Lachenmayer L (2004). "Serotonin neurotoxins--past and present". Neurotox Res. 6 (7–8): 589–614. doi:10.1007/BF03033455. PMID   15639791.
  3. 1 2 Baggott M, Mendelson J (2001). "Does MDMA Cause Brain Damage?". In Holland J (ed.). Ecstasy: The Complete Guide: A Comprehensive Look at the Risks and Benefits of MDMA. Inner Traditions/Bear. pp. 110–145, 396–404. ISBN   978-0-89281-857-0 . Retrieved 24 November 2024. While a single injection of MDMA into the brain (intracerebroventricularly) had no effect on TPH activity, slow infusion of 1 mg/kg MDMA into the brain over 1 hr produced enough oxidative stress to acutely reduce TPH activity (Schmidt and Taylor 1988). The acute decrease in TPH activity is an early effect of MDMA and can be measured at post 15 min (Stone et al. 1989b). TPH inactivation can also be produced by non-neurotoxic MDMA doses (Schmidt and Taylor 1988; Stone et al. 1989a; Stone et al. 1989b). It therefore appears that MDMA rapidly induces oxidative stress but only produces neurotoxicity when endogenous free radical scavenging systems are overwhelmed.
  4. 1 2 Sprague JE, Everman SL, Nichols DE (June 1998). "An integrated hypothesis for the serotonergic axonal loss induced by 3,4-methylenedioxymethamphetamine". Neurotoxicology. 19 (3): 427–441. PMID   9621349.
  5. ↑ Grünblatt E, Mandel S, Youdim MB (April 2000). "MPTP and 6-hydroxydopamine-induced neurodegeneration as models for Parkinson's disease: neuroprotective strategies". J Neurol. 247 (Suppl 2): II95–102. doi:10.1007/pl00022909. PMID   10991672.
  6. ↑ Parrott AC (April 2002). "Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic neurotoxicity". Pharmacol Biochem Behav. 71 (4): 837–844. doi:10.1016/s0091-3057(01)00711-0. PMID   11888574.
  7. ↑ Parrott AC (September 2013). "MDMA, serotonergic neurotoxicity, and the diverse functional deficits of recreational 'Ecstasy' users". Neurosci Biobehav Rev. 37 (8): 1466–1484. doi:10.1016/j.neubiorev.2013.04.016. PMID   23660456.
  8. 1 2 Aguilar MA, García-Pardo MP, Parrott AC (January 2020). "Of mice and men on MDMA: A translational comparison of the neuropsychobiological effects of 3,4-methylenedioxymethamphetamine ('Ecstasy')". Brain Res. 1727: 146556. doi:10.1016/j.brainres.2019.146556. PMID   31734398.
  9. ↑ Montgomery C, Roberts CA (January 2022). "Neurological and cognitive alterations induced by MDMA in humans" (PDF). Exp Neurol. 347: 113888. doi:10.1016/j.expneurol.2021.113888. PMID   34624331.
  10. 1 2 3 4 Biel JH, Bopp BA (1978). "Amphetamines: Structure-Activity Relationships". Stimulants. Boston, MA: Springer US. pp. 1–39. doi:10.1007/978-1-4757-0510-2_1. ISBN   978-1-4757-0512-6.
  11. 1 2 3 4 5 6 7 8 Gibb JW, Johnson M, Elayan I, Lim HK, Matsuda L, Hanson GR (1997). "Neurotoxicity of amphetamines and their metabolites" (PDF). NIDA Res Monogr. 173: 128–145. PMID   9260187.
  12. ↑ Fuller RW, Baker JC (November 1974). "Long-lasting reduction of brain 5-hydroxytryptamine concentration by 3-chloramphetamine and 4-chloroamphetamine in iprindole-treated rats". J Pharm Pharmacol. 26 (11): 912–914. doi:10.1111/j.2042-7158.1974.tb09206.x. PMID   4156568.
  13. 1 2 3 4 5 6 7 Nichols DE, Marona-Lewicka D, Huang X, Johnson MP (1993). "Novel serotonergic agents". Drug des Discov. 9 (3–4): 299–312. PMID   8400010.
  14. 1 2 3 4 5 Oeri HE (May 2021). "Beyond ecstasy: Alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy". J Psychopharmacol. 35 (5): 512–536. doi:10.1177/0269881120920420. PMC   8155739 . PMID   32909493.
  15. 1 2 Seiden LS, Sabol KE (1996). "Methamphetamine and methylenedioxymethamphetamine neurotoxicity: possible mechanisms of cell destruction" (PDF). NIDA Res Monogr. 163: 251–276. PMID   8809863.
  16. 1 2 3 4 Itzhak Y, Achat-Mendes C (May 2004). "Methamphetamine and MDMA (ecstasy) neurotoxicity: 'of mice and men'". IUBMB Life. 56 (5): 249–255. doi:10.1080/15216540410001727699. PMID   15370888.
  17. ↑ Johnson CB, Burroughs RL, Baggott MJ, Davidson CJ, Perrine SA, Baker LE (2022). 314.03 / RR6 - Locomotor stimulant effects and persistent serotonin depletions following [1-Benzofuran-5-yl)-N-methylpropan-2-amine (5-MAPB) treatment in Sprague-Dawley rats. Society for Neuroscience Conference, Nov. 14, 2022, San Diego, CA. 5-MAPB has been marketed as a less neurotoxic analogue of MDMA, but no studies have addressed whether 5-MAPB can cause the long lasting serotonergic changes seen with high or repeated MDMA dosing. [...] Neurochemical analyses indicated a statistically significant reduction in 5‑HT and 5-HIAA in all brain regions assessed 24 hours and two weeks after 6 mg/kg 5‑MAPB, with no statistically significant differences in monoamine levels between 1.2 mg/kg and saline-treated rats. There were also non-significant trends for reductions in striatal dopamine at both time intervals after 6 mg/kg 5-MAPB. These results show that 5-MAPB can dose-dependently produce persistent changes in 5-HT and 5-HIAA that appear analogous to those produced by MDMA.
  18. ↑ McCann UD, Seiden LS, Rubin LJ, Ricaurte GA (August 1997). "Brain serotonin neurotoxicity and primary pulmonary hypertension from fenfluramine and dexfenfluramine. A systematic review of the evidence". JAMA. 278 (8): 666–672. doi:10.1001/jama.1997.03550080076043. PMID   9272900.
  19. ↑ Rothman RB, Baumann MH (April 2002). "Serotonin releasing agents. Neurochemical, therapeutic and adverse effects". Pharmacol Biochem Behav. 71 (4): 825–836. doi:10.1016/s0091-3057(01)00669-4. PMID   11888573.
  20. 1 2 Johnson MP, Nichols DE (May 1990). "Comparative serotonin neurotoxicity of the stereoisomers of fenfluramine and norfenfluramine". Pharmacol Biochem Behav. 36 (1): 105–109. doi:10.1016/0091-3057(90)90133-3. PMID   2140899.
  21. 1 2 3 4 Daziani G, Lo Faro AF, Montana V, Goteri G, Pesaresi M, Bambagiotti G, et al. (March 2023). "Synthetic Cathinones and Neurotoxicity Risks: A Systematic Review". Int J Mol Sci. 24 (7): 6230. doi: 10.3390/ijms24076230 . PMC   10093970 . PMID   37047201.
  22. ↑ Caccia S, Anelli M, Ferrarese A, Fracasso C, Garattini S (March 1993). "The role of d-norfenfluramine in the indole-depleting effect of d-fenfluramine in the rat". Eur J Pharmacol. 233 (1): 71–77. doi:10.1016/0014-2999(93)90350-q. PMID   7682511.
  23. ↑ Harvey JA (June 1978). "Neurotoxic action of halogenated amphetamines". Ann N Y Acad Sci. 305 (1): 289–304. Bibcode:1978NYASA.305..289H. doi:10.1111/j.1749-6632.1978.tb31530.x. PMID   81648.
  24. ↑ Shulgin AT (1978). "Psychotomimetic Drugs: Structure-Activity Relationships". Stimulants. Boston, MA: Springer US. pp. 243–333. doi:10.1007/978-1-4757-0510-2_6. ISBN   978-1-4757-0512-6.
  25. ↑ Iversen L, White M, Treble R (December 2014). "Designer psychostimulants: pharmacology and differences". Neuropharmacology. 87: 59–65. doi:10.1016/j.neuropharm.2014.01.015. PMID   24456744.
  26. 1 2 3 4 Nobin A, Björklund A (June 1978). "Degenerative effects of various neurotoxic indoleamines on central monoamine neurons". Ann N Y Acad Sci. 305: 305–327. doi:10.1111/j.1749-6632.1978.tb31531.x. PMID   360938.
  27. 1 2 Björklund A, Nobin A, Stenevi U (December 1973). "The use of neurotoxic dihydroxytryptamines as tools for morphological studies and localized lesioning of central indolamine neurons". Z Zellforsch Mikrosk Anat. 145 (4): 479–501. doi:10.1007/BF00306720. PMID   4774982.
  28. 1 2 3 4 5 Paterak J, Stefański R (2022). "5,6- and 5,7-Dihydroxytryptamines as Serotoninergic Neurotoxins". Handbook of Neurotoxicity. Cham: Springer International Publishing. pp. 691–717. doi:10.1007/978-3-031-15080-7_76. ISBN   978-3-031-15079-1.
  29. 1 2 Massotti M, Scotti de Carolis A, Longo VG (1974). "Effects of three dihydroxylated derivatives of tryptamine on the behavior and on brain amine content in mice". Pharmacol Biochem Behav. 2 (6): 769–776. doi:10.1016/0091-3057(74)90109-9. PMID   4549398.
  30. ↑ Glennon RA, Dukat MG (December 2023). "α-Ethyltryptamine: A Ratiocinatory Review of a Forgotten Antidepressant". ACS Pharmacol Transl Sci. 6 (12): 1780–1789. doi:10.1021/acsptsci.3c00139. PMC   10714429 . PMID   38093842.
  31. ↑ Huang XM, Johnson MP, Nichols DE (July 1991). "Reduction in brain serotonin markers by alpha-ethyltryptamine (Monase)". Eur J Pharmacol. 200 (1): 187–190. doi:10.1016/0014-2999(91)90686-k. PMID   1722753.
  32. ↑ Sainsbury PD, Kicman AT, Archer RP, King LA, Braithwaite RA (2011). "Aminoindanes--the next wave of 'legal highs'?". Drug Test Anal. 3 (7–8): 479–482. doi:10.1002/dta.318. PMID   21748859.
  33. ↑ Brandt SD, Braithwaite RA, Evans-Brown M, Kicman AT (2013). "Aminoindane Analogues". Novel Psychoactive Substances. Elsevier. pp. 261–283. doi:10.1016/b978-0-12-415816-0.00011-0. ISBN   978-0-12-415816-0.
  34. ↑ Johnson MP, Nichols DE (July 1991). "Combined administration of a non-neurotoxic 3,4-methylenedioxymethamphetamine analogue with amphetamine produces serotonin neurotoxicity in rats". Neuropharmacology. 30 (7): 819–822. doi:10.1016/0028-3908(91)90192-e. PMID   1717873.
  35. ↑ Johnson MP, Conarty PF, Nichols DE (July 1991). "[3H]monoamine releasing and uptake inhibition properties of 3,4-methylenedioxymethamphetamine and p-chloroamphetamine analogues". Eur J Pharmacol. 200 (1): 9–16. doi:10.1016/0014-2999(91)90659-e. PMID   1685125.
  36. ↑ Corkery JM, Elliott S, Schifano F, Corazza O, Ghodse AH (July 2013). "MDAI (5,6-methylenedioxy-2-aminoindane; 6,7-dihydro-5H-cyclopenta[f][1,3]benzodioxol-6-amine; 'sparkle'; 'mindy') toxicity: a brief overview and update". Hum Psychopharmacol. 28 (4): 345–355. doi:10.1002/hup.2298. PMID   23881883.
  37. ↑ Johnson MP, Huang XM, Nichols DE (December 1991). "Serotonin neurotoxicity in rats after combined treatment with a dopaminergic agent followed by a nonneurotoxic 3,4-methylenedioxymethamphetamine (MDMA) analogue". Pharmacol Biochem Behav. 40 (4): 915–922. doi:10.1016/0091-3057(91)90106-c. PMID   1726189.
  38. 1 2 3 4 Igarashi K (1998). "The Possible Role of an Active Metafbollte Derived from the Neuroleptic Agent Haloperidol in Drug-Induced Parkinsonism". Journal of Toxicology: Toxin Reviews. 17 (1): 27–38. doi:10.3109/15569549809006488. ISSN   0731-3837.
  39. 1 2 3 Castagnoli N, Castagnoli KP, Van der Schyf CJ, Usuki E, Igarashi K, Steyn SJ, et al. (1999). "Enzyme-catalyzed bioactivation of cyclic tertiary amines to form potential neurotoxins". Pol J Pharmacol. 51 (1): 31–38. PMID   10389142.
  40. 1 2 Kostrzewa RM (2016). "Perinatal Lesioning and Lifelong Effects of the Noradrenergic Neurotoxin 6-Hydroxydopa". Curr Top Behav Neurosci. Current Topics in Behavioral Neurosciences. 29: 43–50. doi:10.1007/7854_2015_414. ISBN   978-3-319-34134-7. PMID   26660536.
  41. 1 2 Kostrzewa RM, Brus R (1998). "Destruction of catecholamine-containing neurons by 6-hydroxydopa, an endogenous amine oxidase cofactor". Amino Acids. 14 (1–3): 175–179. doi:10.1007/BF01345259. PMID   9871458.
  42. 1 2 3 Varešlija D, Tipton KF, Davey GP, McDonald AG (February 2020). "6-Hydroxydopamine: a far from simple neurotoxin". J Neural Transm (Vienna). 127 (2): 213–230. doi:10.1007/s00702-019-02133-6. PMID   31894418.
  43. ↑ Villa M, Muñoz P, Ahumada-Castro U, Paris I, Jiménez A, Martínez I, et al. (July 2013). "One-electron reduction of 6-hydroxydopamine quinone is essential in 6-hydroxydopamine neurotoxicity". Neurotox Res. 24 (1): 94–101. doi:10.1007/s12640-013-9382-7. PMID   23385626.
  44. 1 2 Glinka Y, Gassen M, Youdim MB (1997). "Mechanism of 6-hydroxydopamine neurotoxicity". Advances in Research on Neurodegeneration. Journal of Neural Transmission. Supplementa. Vol. 50. pp. 55–66. doi:10.1007/978-3-7091-6842-4_7. ISBN   978-3-211-82898-4. PMID   9120425.{{cite book}}: |journal= ignored (help)
  45. ↑ Hernandez-Baltazar D, Zavala-Flores LM, Villanueva-Olivo A (October 2017). "The 6-hydroxydopamine model and parkinsonian pathophysiology: Novel findings in an older model" (PDF). Neurologia. 32 (8): 533–539. doi:10.1016/j.nrl.2015.06.011. PMID   26304655.
  46. ↑ Goldstein DS (February 2020). "The catecholaldehyde hypothesis: where MAO fits in". J Neural Transm (Vienna). 127 (2): 169–177. doi:10.1007/s00702-019-02106-9. PMC   10680281 . PMID   31807952.
  47. ↑ Goldstein DS (June 2021). "The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know". Int J Mol Sci. 22 (11): 5999. doi: 10.3390/ijms22115999 . PMC   8199574 . PMID   34206133.
  48. ↑ Badillo-Ramírez I, Saniger JM, Rivas-Arancibia S (October 2019). "5-S-cysteinyl-dopamine, a neurotoxic endogenous metabolite of dopamine: Implications for Parkinson's disease". Neurochem Int. 129: 104514. doi:10.1016/j.neuint.2019.104514. PMID   31369776.
  49. 1 2 Miyazaki I, Asanuma M (April 2009). "Approaches to prevent dopamine quinone-induced neurotoxicity". Neurochem Res. 34 (4): 698–706. doi:10.1007/s11064-008-9843-1. PMID   18770028.
  50. 1 2 Asanuma M, Miyazaki I, Ogawa N (2003). "Dopamine- or L-DOPA-induced neurotoxicity: the role of dopamine quinone formation and tyrosinase in a model of Parkinson's disease". Neurotox Res. 5 (3): 165–176. doi:10.1007/BF03033137. PMID   12835121.
  51. ↑ Goldstein DS, Sharabi Y (January 2019). "The heart of PD: Lewy body diseases as neurocardiologic disorders". Brain Res. 1702: 74–84. doi:10.1016/j.brainres.2017.09.033. PMC   10712237 . PMID   29030055.
  52. ↑ Chakrabarti S, Bisaglia M (April 2023). "Oxidative Stress and Neuroinflammation in Parkinson's Disease: The Role of Dopamine Oxidation Products". Antioxidants. 12 (4): 955. doi: 10.3390/antiox12040955 . PMC   10135711 . PMID   37107329.
  53. 1 2 3 Cao Y, Li B, Ismail N, Smith K, Li T, Dai R, et al. (November 2021). "Neurotoxicity and Underlying Mechanisms of Endogenous Neurotoxins". Int J Mol Sci. 22 (23): 12805. doi: 10.3390/ijms222312805 . PMC   8657695 . PMID   34884606.
  54. ↑ Kurnik-Łucka M, Panula P, Bugajski A, Gil K (February 2018). "Salsolinol: an Unintelligible and Double-Faced Molecule-Lessons Learned from In Vivo and In Vitro Experiments". Neurotox Res. 33 (2): 485–514. doi:10.1007/s12640-017-9818-6. PMC   5766726 . PMID   29063289.
  55. 1 2 3 Baumgarten HG, Klemm HP, Lachenmayer L, Björklund A, Lovenberg W, Schlossberger HG (June 1978). "Mode and mechanism of action of neurotoxic indoleamines: a review and a progress report". Ann N Y Acad Sci. 305 (1): 3–24. Bibcode:1978NYASA.305....3B. doi:10.1111/j.1749-6632.1978.tb31507.x. PMID   360937.
  56. ↑ Maret G, Testa B, Jenner P, el Tayar N, Carrupt PA (1990). "The MPTP story: MAO activates tetrahydropyridine derivatives to toxins causing parkinsonism". Drug Metab Rev. 22 (4): 291–332. doi:10.3109/03602539009041087. PMID   2253555.
  57. ↑ Manaye KF, Sonsalla PK, Barnett G, Heikkila RE, Woodward DJ, Smith WK, et al. (July 1989). "1-Methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'CH3-MPTP)-induced degeneration of mesostriatal dopaminergic neurons in the mouse: biochemical and neuroanatomical studies". Brain Res. 491 (2): 307–315. doi:10.1016/0006-8993(89)90065-6. PMID   2765888.
  58. ↑ Heikkila RE, Sieber BA, Manzino L, Sonsalla PK (June 1989). "Some features of the nigrostriatal dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse". Mol Chem Neuropathol. 10 (3): 171–183. doi:10.1007/BF03159727. PMID   2669769.
  59. ↑ Youngster SK, Duvoisin RC, Hess A, Sonsalla PK, Kindt MV, Heikkila RE (March 1986). "1-Methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'-CH3-MPTP) is a more potent dopaminergic neurotoxin than MPTP in mice". Eur J Pharmacol. 122 (2): 283–287. doi:10.1016/0014-2999(86)90115-9. PMID   3486770.
  60. ↑ Rose S, Nomoto M, Jackson EA, Gibb WR, Jenner P, Marsden CD (May 1990). "1-Methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine (2'-methyl-MPTP) is less neurotoxic than MPTP in the common marmoset". Eur J Pharmacol. 181 (1–2): 97–103. doi:10.1016/0014-2999(90)90249-6. PMID   2117541.
  61. 1 2 Przedborski S, Vila M (2001). "MPTP: a review of its mechanisms of neurotoxicity". Clinical Neuroscience Research. 1 (6): 407–418. doi:10.1016/S1566-2772(01)00019-6.
  62. ↑ Dinis-Oliveira RJ, Remião F, Carmo H, Duarte JA, Navarro AS, Bastos ML, et al. (December 2006). "Paraquat exposure as an etiological factor of Parkinson's disease". Neurotoxicology. 27 (6): 1110–1122. Bibcode:2006NeuTx..27.1110D. doi:10.1016/j.neuro.2006.05.012. PMID   16815551. Ironically, in the 1960s, MPP+ itself had been tested as an herbicide under the commercial name of cyperquat (Di Monte, 2001).
  63. 1 2 3 4 5 Masato A, Plotegher N, Boassa D, Bubacco L (August 2019). "Impaired dopamine metabolism in Parkinson's disease pathogenesis". Mol Neurodegener. 14 (1): 35. doi: 10.1186/s13024-019-0332-6 . PMC   6728988 . PMID   31488222.
  64. 1 2 3 Arsuffi-Marcon R, Souza LG, Santos-Miranda A, Joviano-Santos JV (March 2024). "Neurotoxicity of Pyrethroids in neurodegenerative diseases: From animals' models to humans' studies". Chem Biol Interact. 391: 110911. Bibcode:2024CBI...39110911A. doi:10.1016/j.cbi.2024.110911. PMID   38367681.
  65. ↑ Xiong J, Zhang X, Huang J, Chen C, Chen Z, Liu L, et al. (March 2016). "Fenpropathrin, a Widely Used Pesticide, Causes Dopaminergic Degeneration". Mol Neurobiol. 53 (2): 995–1008. doi:10.1007/s12035-014-9057-2. PMC   5333774 . PMID   25575680.
  66. ↑ Jiao Z, Wu Y, Qu S (2020). "Fenpropathrin induces degeneration of dopaminergic neurons via disruption of the mitochondrial quality control system". Cell Death Discov. 6: 78. doi:10.1038/s41420-020-00313-y. PMC   7447795 . PMID   32884840.
  67. 1 2 3 4 Bastías-Candia S, Zolezzi JM, Inestrosa NC (February 2019). "Revisiting the Paraquat-Induced Sporadic Parkinson's Disease-Like Model". Mol Neurobiol. 56 (2): 1044–1055. doi:10.1007/s12035-018-1148-z. PMID   29862459.
  68. ↑ Kuter K, Smiałowska M, Wierońska J, Zieba B, Wardas J, Pietraszek M, et al. (June 2007). "Toxic influence of subchronic paraquat administration on dopaminergic neurons in rats". Brain Res. 1155: 196–207. doi:10.1016/j.brainres.2007.04.018. PMID   17493592.
  69. ↑ Goldstein DS, Sullivan P, Cooney A, Jinsmaa Y, Kopin IJ, Sharabi Y (April 2015). "Rotenone decreases intracellular aldehyde dehydrogenase activity: implications for the pathogenesis of Parkinson's disease". J Neurochem. 133 (1): 14–25. doi:10.1111/jnc.13042. PMC   4361358 . PMID   25645689.
  70. ↑ Doorn JA, Florang VR, Schamp JH, Vanle BC (January 2014). "Aldehyde dehydrogenase inhibition generates a reactive dopamine metabolite autotoxic to dopamine neurons". Parkinsonism Relat Disord. 20 Suppl 1 (1): S73–S75. doi:10.1016/S1353-8020(13)70019-1. PMC   3932615 . PMID   24262193.
  71. ↑ Legros H, Dingeval MG, Janin F, Costentin J, Bonnet JJ (March 2004). "Toxicity of a treatment associating dopamine and disulfiram for catecholaminergic neuroblastoma SH-SY5Y cells: relationships with 3,4-dihydroxyphenylacetaldehyde formation". Neurotoxicology. 25 (3): 365–375. Bibcode:2004NeuTx..25..365L. doi:10.1016/S0161-813X(03)00148-7. PMID   15019299.
  72. ↑ Tiernan CT, Edwin EA, Hawong HY, Ríos-Cabanillas M, Goudreau JL, Atchison WD, et al. (April 2015). "Methylmercury impairs canonical dopamine metabolism in rat undifferentiated pheochromocytoma (PC12) cells by indirect inhibition of aldehyde dehydrogenase". Toxicol Sci. 144 (2): 347–356. doi:10.1093/toxsci/kfv001. PMC   4372664 . PMID   25601988.
  73. ↑ Marchitti SA, Deitrich RA, Vasiliou V (June 2007). "Neurotoxicity and metabolism of the catecholamine-derived 3,4-dihydroxyphenylacetaldehyde and 3,4-dihydroxyphenylglycolaldehyde: the role of aldehyde dehydrogenase". Pharmacol Rev. 59 (2): 125–150. doi:10.1124/pr.59.2.1. PMID   17379813.
  74. ↑ Ross SB, Stenfors C (January 2015). "DSP4, a selective neurotoxin for the locus coeruleus noradrenergic system. A review of its mode of action". Neurotox Res. 27 (1): 15–30. doi:10.1007/s12640-014-9482-z. PMID   24964753.
  75. ↑ Jaim-Etcheverry G, Zieher LM (April 1980). "DSP-4: a novel compound with neurotoxic effects on noradrenergic neurons of adult and developing rats". Brain Res. 188 (2): 513–523. doi:10.1016/0006-8993(80)90049-9. PMID   7370771.
  76. ↑ Cagle BS, Crawford RA, Doorn JA (February 2019). "Biogenic Aldehyde-Mediated Mechanisms of Toxicity in Neurodegenerative Disease". Curr Opin Toxicol. 13: 16–21. Bibcode:2019COTox..13...16C. doi:10.1016/j.cotox.2018.12.002. PMC   6625780 . PMID   31304429.
  77. ↑ Matveychuk D, MacKenzie EM, Kumpula D, Song MS, Holt A, Kar S, et al. (January 2022). "Overview of the Neuroprotective Effects of the MAO-Inhibiting Antidepressant Phenelzine". Cell Mol Neurobiol. 42 (1): 225–242. doi:10.1007/s10571-021-01078-3. PMC   8732914 . PMID   33839994.
  78. ↑ Behl T, Kaur D, Sehgal A, Singh S, Sharma N, Zengin G, et al. (June 2021). "Role of Monoamine Oxidase Activity in Alzheimer's Disease: An Insight into the Therapeutic Potential of Inhibitors". Molecules. 26 (12): 3724. doi: 10.3390/molecules26123724 . PMC   8234097 . PMID   34207264.
  79. ↑ Górska A, Marszałł M, Sloderbach A (October 2015). "Neurotoksyczność pirydyniowych metabolitów haloperydolu" [The neurotoxicity of pyridinium metabolites of haloperidol]. Postepy Hig Med Dosw (Online) (in Polish). 69: 1169–1175. doi: 10.5604/17322693.1175009 (inactive 1 November 2024). PMID   26561842.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  80. ↑ Avent KM, Usuki E, Eyles DW, Keeve R, Van der Schyf CJ, Castagnoli N, et al. (1996). "Haloperidol and its tetrahydropyridine derivative (HPTP) are metabolized to potentially neurotoxic pyridinium species in the baboon". Life Sci. 59 (17): 1473–1482. doi:10.1016/0024-3205(96)00475-4. PMID   8890926.
  81. ↑ Avent KM, Riker RR, Fraser GL, Van der Schyf CJ, Usuki E, Pond SM (1997). "Metabolism of haloperidol to pyridinium species in patients receiving high doses intravenously: is HPTP an intermediate?". Life Sci. 61 (24): 2383–2390. doi:10.1016/s0024-3205(97)00955-7. PMID   9399630.
  82. ↑ Ooms F, Delvosal S, Wouters J, Durant F, Dockendolf G, Van't Land C, et al. (2000). "Empirical and molecular modeling study of the pyridinium species RHPP+, an abundant and potentially neurotoxic metabolite of haloperidol". Journal of the Chemical Society, Perkin Transactions 2 (9): 1781–1787. doi:10.1039/b002357o.
  83. ↑ Avent KM, DeVoss JJ, Gillam EM (July 2006). "Cytochrome P450-mediated metabolism of haloperidol and reduced haloperidol to pyridinium metabolites". Chem Res Toxicol. 19 (7): 914–920. doi:10.1021/tx0600090. PMID   16841959.
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