Component
Dopamine
Dopamine
13 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Expressed human DDC decarboxylated L-DOPA; added PLP enhanced the measured activity.
Experimental context and source evidence
- experimental_model
- Human DDC expressed in monkey COS cells; enzyme assays
- exposure
- PLP addition to transfected COS-cell enzyme incubations.
- limitations
- An expression-system response is not proof that supplements increase brain monoamines.
- nutrient_topic
- Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
- organism
- Human DDC expressed in monkey COS cells
- plain_language
- B6 cofactor supports this monoamine-producing step.
- primary_references
- [sumi-1990-ddc] Characterization of recombinant human aromatic L-amino acid decarboxylase expressed in COS cells (1990). https://doi.org/10.1111/j.1471-4159.1990.tb04601.x DOI: 10.1111/j.1471-4159.1990.tb04601.x
- tissue_or_cell_type
- COS-cell expression system
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 999–1009
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DDC expressed in monkey COS cells; enzyme assays · source_derived_draft · unverified_draft
### b6-neuro-ddc-dopamine Expressed human DDC decarboxylated L-DOPA; added PLP enhanced the measured activity. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: B6 cofactor supports this monoamine-producing step. organism: Human DDC expressed in monkey COS cells tissue_or_cell_type: COS-cell expression system experimental_model: Human DDC expressed in monkey COS cells; enzyme assays limitations: An expression-system response is not proof that supplements increase brain monoamines. exposure: PLP addition to transfected COS-cell enzyme incubations. [sumi-1990-ddc] Characterization of recombinant human aromatic L-amino acid decarboxylase expressed in COS cells (1990). https://doi.org/10.1111/j.1471-4159.1990.tb04601.x DOI: 10.1111/j.1471-4159.1990.tb04601.x
Complete structured claim and evidence
Where it participates (unsigned role)
Human DBH is the copper-enzyme step converting dopamine to norepinephrine; the study resolved its catalytic-core architecture.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/27152332.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "984a9036d5157e29cdef55d42201887d3ff43cf533185148ba4e3f5c143ced09", "start_char": 0, "end_char": 1325, "text_sha256": "984a9036d5157e29cdef55d42201887d3ff43cf533185148ba4e3f5c143ced09"}
- experimental_model
- Human DBH X-ray crystallography
- exposure
- Crystal structure at 2.9 angstrom resolution
- limitations
- Open and closed conformations were observed; the proposed catalytic alternation and fully occupied binuclear states require further evidence. Do not equate a structural model with proof of psychiatric effects from copper intake.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human protein
- plain_language
- Copper is part of the enzyme that converts one neurotransmitter into another.
- primary_references
- [copper-p27152332] The crystal structure of human dopamine β-hydroxylase at 2.9 Å resolution. (2016). https://pubmed.ncbi.nlm.nih.gov/27152332/ DOI: 10.1126/sciadv.1500980
- tissue_or_cell_type
- Purified dimeric enzyme
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1079–1090
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DBH X-ray crystallography · source_derived_draft · unverified_draft
### copper-dbh-neurotransmitter-step Human DBH is the copper-enzyme step converting dopamine to norepinephrine; the study resolved its catalytic-core architecture. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper is part of the enzyme that converts one neurotransmitter into another. organism: Human protein tissue_or_cell_type: Purified dimeric enzyme experimental_model: Human DBH X-ray crystallography limitations: Open and closed conformations were observed; the proposed catalytic alternation and fully occupied binuclear states require further evidence. Do not equate a structural model with proof of psychiatric effects from copper intake. exposure: Crystal structure at 2.9 angstrom resolution evidence_span: {"source_cache": "artifacts/copper-research/27152332.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "984a9036d5157e29cdef55d42201887d3ff43cf533185148ba4e3f5c143ced09", "start_char": 0, "end_char": 1325, "text_sha256": "984a9036d5157e29cdef55d42201887d3ff43cf533185148ba4e3f5c143ced09"} [copper-p27152332] The crystal structure of human dopamine β-hydroxylase at 2.9 Å resolution. (2016). https://pubmed.ncbi.nlm.nih.gov/27152332/ DOI: 10.1126/sciadv.1500980
Complete structured claim and evidenceBacterial tyrosine decarboxylases converted levodopa to dopamine despite competing tyrosine or human decarboxylase inhibitors.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Bacterial enzyme experiments, human PD associations and proximal-intestinal rat studies.
- limitations
- Patient abundance associations and rat plasma effects are not proof that changing dietary tyrosine improves levodopa response.
- nutrient_topic
- L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
- plain_language
- Blocking the human enzyme may leave a microbial route active.
- primary_references
- Gut bacterial tyrosine decarboxylases restrict levels of levodopa in the treatment of Parkinson's disease. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30659181/ · DOI 10.1038/s41467-019-08294-y
L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 340–346
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Bacterial enzyme experiments, human PD associations and proximal-intestinal rat studies. · source_derived_draft · unverified_draft
## l-tyrosine-bacterial-drug Blocking the human enzyme may leave a microbial route active. Bacterial tyrosine decarboxylases converted levodopa to dopamine despite competing tyrosine or human decarboxylase inhibitors. Model: Bacterial enzyme experiments, human PD associations and proximal-intestinal rat studies. Limitations: Patient abundance associations and rat plasma effects are not proof that changing dietary tyrosine improves levodopa response. Evidence access: Primary abstract Gut bacterial tyrosine decarboxylases restrict levels of levodopa in the treatment of Parkinson's disease. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30659181/ · DOI 10.1038/s41467-019-08294-y
Complete structured claim and evidenceCombined phenylalanine/tyrosine depletion decreased dopamine-transient frequency without decreasing transient amplitude in freely moving rats.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Fast-scan cyclic voltammetry in a separate rat group from the tissue-content experiment.
- limitations
- The release endpoint is not a direct human measurement; the corrected norepinephrine endpoint is excluded. Correction record: The 2018 correction (PMID 30094500) reports an error in norepinephrine standard concentrations used for HPLC calibration. The correction abstract was inspected, but full notice content was unavailable; its complete quantitative scope remains unverified. This collection uses the tyrosine depletion and dopamine-transient findings and does not reuse the original norepinephrine concentration result. https://pubmed.ncbi.nlm.nih.gov/30094500/
- nutrient_topic
- L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
- plain_language
- Less precursor can change release dynamics without simply emptying all dopamine stores.
- primary_references
- Acute phenylalanine/tyrosine depletion of phasic dopamine in the rat brain. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26944052/ · DOI 10.1007/s00213-016-4259-0
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 388–394
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fast-scan cyclic voltammetry in a separate rat group from the tissue-content experiment. · source_derived_draft · unverified_draft
## l-tyrosine-rat-dopamine-transients Less precursor can change release dynamics without simply emptying all dopamine stores. Combined phenylalanine/tyrosine depletion decreased dopamine-transient frequency without decreasing transient amplitude in freely moving rats. Model: Fast-scan cyclic voltammetry in a separate rat group from the tissue-content experiment. Limitations: The release endpoint is not a direct human measurement; the corrected norepinephrine endpoint is excluded. Correction record: The 2018 correction (PMID 30094500) reports an error in norepinephrine standard concentrations used for HPLC calibration. The correction abstract was inspected, but full notice content was unavailable; its complete quantitative scope remains unverified. This collection uses the tyrosine depletion and dopamine-transient findings and does not reuse the original norepinephrine concentration result. https://pubmed.ncbi.nlm.nih.gov/30094500/ Evidence access: Primary abstract Acute phenylalanine/tyrosine depletion of phasic dopamine in the rat brain. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26944052/ · DOI 10.1007/s00213-016-4259-0
Complete structured claim and evidenceTartrazine inhibited dopamine sulfation in human liver cytosol.
Experimental context and source evidence
- dose
- Tartrazine in an additive-inhibition panel; concentration and substrate amounts not in abstract
- duration
- Assay interval not specified in accessed abstract
- evidence_access
- Primary PubMed abstract; unrecovered method details explicitly retained.
- evidence_scope
- literature_reviewed; source-specific experimental curation
- experimental_model
- Human liver cytosolic preparations
- limitations
- A functional sulfation assay does not demonstrate direct SULT1A3 binding or altered human brain dopamine. Ethinyloestradiol findings for other additives are not transferred to tartrazine.
- nutrient_topic
- Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
- organism
- Human liver cytosolic preparations
- plain_language
- Tartrazine inhibited dopamine sulfation in human liver cytosol.
- primary_references
- Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases. (1993). https://pubmed.ncbi.nlm.nih.gov/8250957/ DOI: 10.1016/0006-2952(93)90575-h
- route
- In vitro cytosolic enzyme assay
- tissue
- Dopamine sulfation
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 259–268
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Human liver cytosolic preparations · source_derived_draft · unverified_draft
## tartrazine-dopamine-sulfation Tartrazine inhibited dopamine sulfation in human liver cytosol. Model/species: Human liver cytosolic preparations Tissue: Dopamine sulfation Exposure: Tartrazine in an additive-inhibition panel; concentration and substrate amounts not in abstract Route: In vitro cytosolic enzyme assay Duration: Assay interval not specified in accessed abstract Limits: A functional sulfation assay does not demonstrate direct SULT1A3 binding or altered human brain dopamine. Ethinyloestradiol findings for other additives are not transferred to tartrazine. Primary reference: Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases. (1993). https://pubmed.ncbi.nlm.nih.gov/8250957/ DOI: 10.1016/0006-2952(93)90575-h Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidenceTheanine protected SH-SY5Y cells against the injury produced by dopamine plus copper.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/39499422.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4", "start_char": 0, "end_char": 1871, "text_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4"}
- experimental_model
- Cell-free oxidation and cultured-cell injury assays
- exposure
- Dopamine with and without copper; theanine concentration-ratio experiments
- limitations
- High experimental substrate ratios; no human copper-depletion, Parkinson disease treatment or systemic chelation conclusion. Cellular protection does not establish effective brain exposure.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Human SH-SY5Y cell line and chemical systems
- plain_language
- Cell survival was measured separately from the chemical oxidation assay.
- primary_references
- [theanine-p39499422] L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities. (2025). https://pubmed.ncbi.nlm.nih.gov/39499422/ DOI: 10.1007/s12035-024-04601-x
- tissue_or_cell_type
- Copper-facilitated dopamine oxidation
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 744–755
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free oxidation and cultured-cell injury assays · source_derived_draft · unverified_draft
### theanine-copper-cell-protection Theanine protected SH-SY5Y cells against the injury produced by dopamine plus copper. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cell survival was measured separately from the chemical oxidation assay. organism: Human SH-SY5Y cell line and chemical systems tissue_or_cell_type: Copper-facilitated dopamine oxidation experimental_model: Cell-free oxidation and cultured-cell injury assays limitations: High experimental substrate ratios; no human copper-depletion, Parkinson disease treatment or systemic chelation conclusion. Cellular protection does not establish effective brain exposure. exposure: Dopamine with and without copper; theanine concentration-ratio experiments evidence_span: {"source_cache": "artifacts/theanine-research/39499422.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4", "start_char": 0, "end_char": 1871, "text_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4"} [theanine-p39499422] L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities. (2025). https://pubmed.ncbi.nlm.nih.gov/39499422/ DOI: 10.1007/s12035-024-04601-x
Complete structured claim and evidenceTheanine suppressed copper-facilitated dopamine oxidation; the authors attributed this to copper chelation.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/39499422.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4", "start_char": 0, "end_char": 1871, "text_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4"}
- experimental_model
- Cell-free oxidation and cultured-cell injury assays
- exposure
- Dopamine with and without copper; theanine concentration-ratio experiments
- limitations
- High experimental substrate ratios; no human copper-depletion, Parkinson disease treatment or systemic chelation conclusion. Cellular protection does not establish effective brain exposure.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Human SH-SY5Y cell line and chemical systems
- plain_language
- Copper changed the chemistry of dopamine oxidation, and theanine interfered with that chemistry in the assay.
- primary_references
- [theanine-p39499422] L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities. (2025). https://pubmed.ncbi.nlm.nih.gov/39499422/ DOI: 10.1007/s12035-024-04601-x
- tissue_or_cell_type
- Copper-facilitated dopamine oxidation
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 731–742
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free oxidation and cultured-cell injury assays · source_derived_draft · unverified_draft
### theanine-copper-dopamine-oxidation Theanine suppressed copper-facilitated dopamine oxidation; the authors attributed this to copper chelation. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper changed the chemistry of dopamine oxidation, and theanine interfered with that chemistry in the assay. organism: Human SH-SY5Y cell line and chemical systems tissue_or_cell_type: Copper-facilitated dopamine oxidation experimental_model: Cell-free oxidation and cultured-cell injury assays limitations: High experimental substrate ratios; no human copper-depletion, Parkinson disease treatment or systemic chelation conclusion. Cellular protection does not establish effective brain exposure. exposure: Dopamine with and without copper; theanine concentration-ratio experiments evidence_span: {"source_cache": "artifacts/theanine-research/39499422.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4", "start_char": 0, "end_char": 1871, "text_sha256": "abb7a869056bc8c43d6792b2a4ff9a1b15738facf454daeb3f92df383932b9c4"} [theanine-p39499422] L-Theanine Effectively Protects Against Copper-Facilitated Dopamine Oxidation: Implication for Relieving Dopamine Overflow-Associated Neurotoxicities. (2025). https://pubmed.ncbi.nlm.nih.gov/39499422/ DOI: 10.1007/s12035-024-04601-x
Complete structured claim and evidenceStrychnine reduced the theanine-induced dopamine response in rat striatum.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/18196445.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59fdaf94d59c2f4b2981c29cd2981c043351aae1299a59a19e29979076957839", "start_char": 0, "end_char": 1118, "text_sha256": "59fdaf94d59c2f4b2981c29cd2981c043351aae1299a59a19e29979076957839"}
- experimental_model
- In-vivo striatal microdialysis with receptor antagonists
- exposure
- Local brain theanine administration; glycine and AMPA antagonists
- limitations
- Direct brain dosing bypasses oral absorption and blood-brain-barrier transport. Antagonist sensitivity identifies pathway involvement, not necessarily direct theanine binding.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Conscious rats
- plain_language
- The glycine-receptor pathway participated in the dopamine response.
- primary_references
- [theanine-p18196445] Theanine, gamma-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats. (2009). https://pubmed.ncbi.nlm.nih.gov/18196445/ DOI: 10.1007/s00726-007-0020-7
- tissue_or_cell_type
- Striatal extracellular neurotransmitters
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 380–391
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vivo striatal microdialysis with receptor antagonists · source_derived_draft · unverified_draft
### theanine-glycine-dopamine Strychnine reduced the theanine-induced dopamine response in rat striatum. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glycine-receptor pathway participated in the dopamine response. organism: Conscious rats tissue_or_cell_type: Striatal extracellular neurotransmitters experimental_model: In-vivo striatal microdialysis with receptor antagonists limitations: Direct brain dosing bypasses oral absorption and blood-brain-barrier transport. Antagonist sensitivity identifies pathway involvement, not necessarily direct theanine binding. exposure: Local brain theanine administration; glycine and AMPA antagonists evidence_span: {"source_cache": "artifacts/theanine-research/18196445.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59fdaf94d59c2f4b2981c29cd2981c043351aae1299a59a19e29979076957839", "start_char": 0, "end_char": 1118, "text_sha256": "59fdaf94d59c2f4b2981c29cd2981c043351aae1299a59a19e29979076957839"} [theanine-p18196445] Theanine, gamma-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats. (2009). https://pubmed.ncbi.nlm.nih.gov/18196445/ DOI: 10.1007/s00726-007-0020-7
Complete structured claim and evidenceAscorbate is the presumed in vivo reductant of dopamine beta-monooxygenase; the one-electron reductant ferrocyanide was nearly as kinetically competent, while dopamine as sole reductant reduced enzymic copper in a rate-limiting step 40-fold slower than with ascorbate, and the reductant binds at a site physically distinct from the substrate site.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/cold-research/3676254.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e929132eed0f1c94ab0bdbef6e31bca7ecbed222cf9b585e17a1cfae7e93c82a", "start_char": 0, "end_char": 1648, "text_sha256": "e929132eed0f1c94ab0bdbef6e31bca7ecbed222cf9b585e17a1cfae7e93c82a"}
- experimental_model
- Steady-state kinetics of dopamine beta-monooxygenase with structurally distinct reductants
- exposure
- Ascorbate, ferrocyanide or dopamine itself as the reducing agent, with deuterium isotope effects
- limitations
- A kinetic comparison identifying ascorbate as the presumed physiological reductant and locating a separate binding site for it. Truncated abstract; the reductant site is inferred from kinetics and modelling.
- nutrient_topic
- Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
- organism
- Bovine enzyme
- plain_language
- Vitamin C is what hands the enzyme back its electrons, and without it the reaction crawls.
- primary_references
- [cold-p3676254] Characterization of alternate reductant binding and electron transfer in the dopamine beta-monooxygenase reaction. (1987). https://pubmed.ncbi.nlm.nih.gov/3676254/ DOI: 10.1021/bi00391a013
- tissue_or_cell_type
- Purified enzyme
Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 585–596
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Steady-state kinetics of dopamine beta-monooxygenase with structurally distinct reductants · source_derived_draft · unverified_draft
### cold-ascorbate-reductant Ascorbate is the presumed in vivo reductant of dopamine beta-monooxygenase; the one-electron reductant ferrocyanide was nearly as kinetically competent, while dopamine as sole reductant reduced enzymic copper in a rate-limiting step 40-fold slower than with ascorbate, and the reductant binds at a site physically distinct from the substrate site. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Vitamin C is what hands the enzyme back its electrons, and without it the reaction crawls. organism: Bovine enzyme tissue_or_cell_type: Purified enzyme experimental_model: Steady-state kinetics of dopamine beta-monooxygenase with structurally distinct reductants limitations: A kinetic comparison identifying ascorbate as the presumed physiological reductant and locating a separate binding site for it. Truncated abstract; the reductant site is inferred from kinetics and modelling. exposure: Ascorbate, ferrocyanide or dopamine itself as the reducing agent, with deuterium isotope effects evidence_span: {"source_cache": "artifacts/cold-research/3676254.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e929132eed0f1c94ab0bdbef6e31bca7ecbed222cf9b585e17a1cfae7e93c82a", "start_char": 0, "end_char": 1648, "text_sha256": "e929132eed0f1c94ab0bdbef6e31bca7ecbed222cf9b585e17a1cfae7e93c82a"} [cold-p3676254] Characterization of alternate reductant binding and electron transfer in the dopamine beta-monooxygenase reaction. (1987). https://pubmed.ncbi.nlm.nih.gov/3676254/ DOI: 10.1021/bi00391a013
Complete structured claim and evidenceDopamine beta-hydroxylase specifically binds 8 moles of copper per mole of tetramer, confirmed by radiolabel, atomic absorption, NMR and EPR titration, and catalytic rate increased with copper up to that ratio and was constant thereafter, so this stoichiometry is required for maximal activity.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/cold-research/6323422.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dac85ce0ad7c7d5994b97d55b129050a0e7ca8bf96943578d272054db6a07a62", "start_char": 0, "end_char": 1346, "text_sha256": "dac85ce0ad7c7d5994b97d55b129050a0e7ca8bf96943578d272054db6a07a62"}
- experimental_model
- Copper titration of bovine adrenal dopamine beta-hydroxylase followed by NMR, EPR and inhibitor kinetics
- exposure
- Titration with copper and measurement of catalytic rate
- limitations
- Stoichiometry measured three independent ways. It establishes how much copper the enzyme needs, not how much copper a person needs.
- nutrient_topic
- Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
- organism
- Bovine enzyme
- plain_language
- The enzyme that turns dopamine into noradrenaline needs exactly eight copper atoms to work fully.
- primary_references
- [cold-p6323422] Kinetic and spectroscopic studies of the interaction of copper with dopamine beta-hydroxylase. (1984). https://pubmed.ncbi.nlm.nih.gov/6323422/ DOI: 10.1016/s0021-9258(17)43105-x
- tissue_or_cell_type
- Adrenal medulla enzyme
Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 559–570
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper titration of bovine adrenal dopamine beta-hydroxylase followed by NMR, EPR and inhibitor kinetics · source_derived_draft · unverified_draft
### cold-dbh-copper-stoichiometry Dopamine beta-hydroxylase specifically binds 8 moles of copper per mole of tetramer, confirmed by radiolabel, atomic absorption, NMR and EPR titration, and catalytic rate increased with copper up to that ratio and was constant thereafter, so this stoichiometry is required for maximal activity. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The enzyme that turns dopamine into noradrenaline needs exactly eight copper atoms to work fully. organism: Bovine enzyme tissue_or_cell_type: Adrenal medulla enzyme experimental_model: Copper titration of bovine adrenal dopamine beta-hydroxylase followed by NMR, EPR and inhibitor kinetics limitations: Stoichiometry measured three independent ways. It establishes how much copper the enzyme needs, not how much copper a person needs. exposure: Titration with copper and measurement of catalytic rate evidence_span: {"source_cache": "artifacts/cold-research/6323422.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dac85ce0ad7c7d5994b97d55b129050a0e7ca8bf96943578d272054db6a07a62", "start_char": 0, "end_char": 1346, "text_sha256": "dac85ce0ad7c7d5994b97d55b129050a0e7ca8bf96943578d272054db6a07a62"} [cold-p6323422] Kinetic and spectroscopic studies of the interaction of copper with dopamine beta-hydroxylase. (1984). https://pubmed.ncbi.nlm.nih.gov/6323422/ DOI: 10.1016/s0021-9258(17)43105-x
Complete structured claim and evidenceGlutamate co-entry increased vesicular acidification in the study, supporting the pH gradient used for monoamine storage.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rodent synaptic-vesicle acidification assays; glutamate compared with chloride.
- limitations
- The preparation does not show that glutamate supplements increase human dopamine.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- One transmitter can influence storage of another through shared vesicle chemistry.
- primary_references
- Vesicular glutamate transport promotes dopamine storage and glutamate corelease in vivo. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20223200/ · DOI 10.1016/j.neuron.2010.02.012
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 314–320
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rodent synaptic-vesicle acidification assays; glutamate compared with chloride. · source_derived_draft · unverified_draft
## glutamate-glutamate-vesicle-acidification One transmitter can influence storage of another through shared vesicle chemistry. Glutamate co-entry increased vesicular acidification in the study, supporting the pH gradient used for monoamine storage. Model: Rodent synaptic-vesicle acidification assays; glutamate compared with chloride. Limitations: The preparation does not show that glutamate supplements increase human dopamine. Evidence access: Primary full text Vesicular glutamate transport promotes dopamine storage and glutamate corelease in vivo. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20223200/ · DOI 10.1016/j.neuron.2010.02.012
Complete structured claim and evidenceDopamine-neuron Slc17a6 deletion reduced dopamine stores in ventral-striatal projections and reduced cocaine-stimulated locomotor responses while sparing baseline motor behavior.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse conditional knockout with tissue dopamine and behavioral measurements.
- limitations
- Multiple downstream effects coexist; this does not prove every dopamine neuron or behavior depends equally on VGLUT2.
- nutrient_topic
- L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
- plain_language
- Removing the glutamate-loading route changed another transmitter system in a specific circuit.
- primary_references
- Vesicular glutamate transport promotes dopamine storage and glutamate corelease in vivo. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20223200/ · DOI 10.1016/j.neuron.2010.02.012
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 322–328
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse conditional knockout with tissue dopamine and behavioral measurements. · source_derived_draft · unverified_draft
## glutamate-vglut2-dopamine-stores Removing the glutamate-loading route changed another transmitter system in a specific circuit. Dopamine-neuron Slc17a6 deletion reduced dopamine stores in ventral-striatal projections and reduced cocaine-stimulated locomotor responses while sparing baseline motor behavior. Model: Mouse conditional knockout with tissue dopamine and behavioral measurements. Limitations: Multiple downstream effects coexist; this does not prove every dopamine neuron or behavior depends equally on VGLUT2. Evidence access: Primary full text Vesicular glutamate transport promotes dopamine storage and glutamate corelease in vivo. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20223200/ · DOI 10.1016/j.neuron.2010.02.012
Complete structured claim and evidenceEthanol preferentially stimulated dopamine release in the nucleus accumbens of freely moving rats.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/alcohol-research/3761194.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98cf7c1ea1f6fbf3da6b89ab6beaed01a679ea1c8d4823f00952692a0c9203ca", "start_char": 0, "end_char": 1539, "text_sha256": "98cf7c1ea1f6fbf3da6b89ab6beaed01a679ea1c8d4823f00952692a0c9203ca"}
- experimental_model
- In vivo microdialysis in freely moving rats
- exposure
- Ethanol administration with regional dopamine measurement
- limitations
- A reward-pathway measurement in freely moving animals. Dopamine release is a correlate of reinforcement, not a measure of liking or dependence.
- nutrient_topic
- Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
- organism
- Rat
- plain_language
- Alcohol raises dopamine in the brain region that marks things as worth repeating.
- primary_references
- [alcohol-p3761194] Preferential stimulation of dopamine release in the nucleus accumbens of freely moving rats by ethanol. (1986). https://pubmed.ncbi.nlm.nih.gov/3761194/ DOI: 10.1016/s0022-3565(25)23929-5
- tissue_or_cell_type
- Nucleus accumbens
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 423–434
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo microdialysis in freely moving rats · source_derived_draft · unverified_draft
### alcohol-accumbens-dopamine Ethanol preferentially stimulated dopamine release in the nucleus accumbens of freely moving rats. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Alcohol raises dopamine in the brain region that marks things as worth repeating. organism: Rat tissue_or_cell_type: Nucleus accumbens experimental_model: In vivo microdialysis in freely moving rats limitations: A reward-pathway measurement in freely moving animals. Dopamine release is a correlate of reinforcement, not a measure of liking or dependence. exposure: Ethanol administration with regional dopamine measurement evidence_span: {"source_cache": "artifacts/alcohol-research/3761194.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98cf7c1ea1f6fbf3da6b89ab6beaed01a679ea1c8d4823f00952692a0c9203ca", "start_char": 0, "end_char": 1539, "text_sha256": "98cf7c1ea1f6fbf3da6b89ab6beaed01a679ea1c8d4823f00952692a0c9203ca"} [alcohol-p3761194] Preferential stimulation of dopamine release in the nucleus accumbens of freely moving rats by ethanol. (1986). https://pubmed.ncbi.nlm.nih.gov/3761194/ DOI: 10.1016/s0022-3565(25)23929-5
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.