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Dopamine Oxidation
Submitted by: Asmita Singh
Roll no.: 26
Group: 01
ROL E OF METAL IONS I N
DOPAMI NE OXIDAT ION
TABLE OF CONTENTS
1. Introduction
2. Dopamine
3. Parkinson’s Disease
4. Lab Experiment
5. Requirements
6. Procedure
6.1 Reaction Between Mn2+ And DA
6.2 Reaction Between Cu2+ And DA
6.3 Oxidation Of DA
7. Observations
8. Analysis Of The Spectra
9. Postlaboratory Activity
10. What I Have Learnt
11. References
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1: INTRODUCTION
This power point includes the experiment by which we
can evaluate the role of some metal ions i.e., Cu(II) and
Mn(II) in dopamine oxidation, related to Parkinsonism.
In the experiment reactions are carried out at
physiological temperature (or possibly at room
temperature), with common or inexpensive laboratory
materials and with only a UV−vis spectrophotometer as
more complex instrumentation.
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2: DOPAMINE
• Dopamine (DA) is a monoamine neurotransmitter that is produced in the substantia nigra,
ventral tegmental area (VTA), and hypothalamus of the brain.
• It is also known as “Feel Good Chemical” or “Pleasure Chemical” because it plays an essential role
in the brain’s reward system, where it reinforces the feelings of pleasure that people experience when they
engage in rewarding activities.
4-(2-aminoethyl)benzene-1,2-diol
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DOPAMINE OXI DAT I ON DOPAMINE IS SYNTHESIZED FROM AMINO ACID TYROSINE VIA TWO
ENZYMATIC STEPS THAT OCCUR IN THE CYTOSOL:
• In the first step the amino acid L-tyrosine is converted into L-3,4-dihydroxyphenylalanine (L-DOPA) via
tyrosine hydroxylase (TH).
• In the second step, L-DOPA is converted to dopamine via aromatic amino acid decarboxylase (AADC)
Once DA is synthesized, it is stored in vesicles within the nerve cells and when a nerve impulse
reaches the end of a nerve fiber, dopamine is released into the synapse, which is the small gap between
two nerve cells. After being released it binds to the dopamine receptors on neighboring nerve cells and
transmit signals across the synapse.
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After DA has transmitted its signal, it is removed from the synapse by reuptake back into the nerve cell that
released it.The reuptake process is mediated by specific proteins called dopamine transporters.
Once DA is back inside the nerve cell, it can be broken down by enzymes such as monoamine oxidase (MAO)
and catechol-O-methyltransferase (COMT), which convert dopamine into other substances that can be eliminated
from the body.
The balance of dopamine synthesis, release, and breakdown is crucial for proper brain function, and disruptions
to this balance have been implicated in a number of neurological and psychiatric disorders,
such as Parkinson's disease, schizophrenia and addiction.
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3: PARKINSON’S DISEASE
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• Parkinson’s disease is a slowly progressive disease caused by the loss of dopamine brain cells
(neurons).
• Although the exact cause of PD is still unknown,
but it is believed that both hereditary and
environmental factors are involved in the disorder.
• The role of metals in PD has been hypothesized
based on observational studies evaluating
occupational and environmental expositions.
• Prolonged exposure to copper and manganese has been linked to an increased risk of Parkinson's
disease.
• Parkinsonism is one of the symptoms of Wilson's disease, which is caused by copper accumulation,
• Manganese has also been associated with the development of several kinds of Parkinsonism. Mn 2+ is
able to react with superoxide radicals generating hydrogen peroxide and the strong oxidizing agent
Mn3+.
DOPAMINE OXIDATION TO AMINOCHROME
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Dopamine being a good metal chelator it coordinates and reduces metals such as Cu 2+ and Mn2+ and setting up the
conditions of generation of damaging reactive oxygen species(ROS).
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4: LAB EXPERIMENT
• The experiment's main activity is focused to determining how two redox metals contribute to the
degradation of DA.
• In particular, a simplified model of the effect of Mn2+ and Cu2+ ions on the oxidation of DA will be
studied in the absence and in the presence of the chelating agent EDTA (2,2′,2″,2‴-(ethane-1,2-
diyldinitrilo)tetraacetic acid, better known as ethylenediaminetetraacetic acid), usually employed
to grab toxic metals.
• This experiment consists of the study of the oxidation of DA, DA + M(II) , and DA + M(II) +
EDTA (with M(II) = Cu(II) and Mn(II) ), by means of UV−vis spectrophotometry.
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5: REQUIREMENTS
ROL E OF METAL IONS I N
DOPAMI NE OXIDAT ION
A PPA R AT U S REQ U I R ED CH EM I CA LS RE Q U I R ED
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6: PROCEDURE
6.1: Reaction between Mn2+ and DA
Experiment 1: absence of EDTA
Fixed volumes of solutions A and B were mixed ([Mn] final =
200μM, [DA]final = 100μM), and the resulting mixture's UV-vis
spectra were recorded between 200 and 800 nm at 37 °C every
The following solutions were prepared as a five minutes until substantial changes were no longer visible.
starting point:
(A) a 1 mM solution of DA·HCl in PB,
(B) a 0.5 mM solution of MnSO4·H2O in PB, and
(C) a 0.5 mM solution of MnSO4· H2O and 0.5 mM
of EDTA in PB.
Experiment 2: presence of EDTA
This experiment consists of mixing fixed volumes of solutions
A and C ([Mn-EDTA]final = 200 μM, [DA]final = 100 μM) and
recording the UV−vis spectra in the same way as experiment 1
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6.2: Reaction between Cu2+ and DA
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6.3: Oxidation Of DA
NOTE: Without the buffering capacity of phosphate buffer, the pH of the solution may be more
susceptible to fluctuations caused by changes in temperature or exposure to air. This could lead
to inconsistent or unstable results when using the solution for experiments or analyses.
Therefore, it is generally recommended to use a buffer, such as phosphate buffer, when
preparing copper-dopamine solutions.
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DOPAMI NE OXIDAT ION 7: OBSERTVATIONS:
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8: ANALYSIS OF THE SPECTRA
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9: POSTLABORATORY ACTIVITY
From each spectrum of the Mn(II) and Cu(II) series,
A303 (i.e., the absorbance measured at λ = 303 nm) and
A800 (i.e., the absorbance measured at λ = 800 nm) were recorded.
A graph reporting [(A303 − A800) − (A303,t0 − A800,t0)] vs reaction time t,
where A303,t0 and A800,t0 are the absorbance values measured at t = 0,
provides a more visually clear summary of the results.
1: Knowledge and understanding of the effects of some metal ions on the oxidation
of DA.
2: Reinforcement of prior knowledge about UV- vis spectroscopy, redox reactions,
metal complexes.
3: Learnt how dopamine levels affects our bodies.
4: Our physical and mental health might be negatively impacted by dopamine level
imbalance.
11. REFERENCES
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• Ravera M.; Gabano E.; Role of metals ion in the dopamine oxidation, J. Chem. Educ. 2021, 98, 4031−4036
• https://www.verywellmind.com/what-is-dopamine-5185621
• https://www.biorxiv.org/content/10.1101/2020.10.26.354688v1.full
• https://www.thegoldenconcepts.com/blogs/health/parkinson-s-disease-spotting-symptoms-preventative-measures
• Segura-Aguilar J.; Paris I.; Muñoz P.; Ferrari E.; zecca L.; Zucca A. F.; Protective and toxic roles of dopamine
in Parkinson’s disease J. Neurochem (2014), 129, 898–915
• Oikawa, S.; Hirosawa, I.; Tada-Oikawa, S.; Furukawa, A.; Nishiura, K.; Kawanishi, S. Mechanism for
manganese enhancement of dopamine-induced oxidative DNA damage and neuronal cell death.
Free Radical Biol. Med. 2006, 41 (5), 748−756.
• Florence T. M.; Stauber J. L. Manganese catalysis of dopamine oxidation The Science of the Total Environment,
78 (1989) 233-240
• Breczko, J.; Plonska-Brzezinska, M. E.; Echegoyen, L. Electrochemical Oxidation and Determination of Dopamine
in the Presence of Uric and Ascorbic Acids Using a Carbon Nano-Onion and Poly(Diallyldimethylammonium
Chloride) Composite. Electrochimica Acta 2012, 72, 61–67.
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