Component

cystine uptake

Independent entity for contextual scientific-audit claims; no universal nutritional effect implied.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Diethyl maleate induced xCT expression and increased cystine uptake in U87 cells.

    SLC7A11 → cystine uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/11406111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7118afd8c6055ed926ee24dbb7a07538f676163d605115ae0d32d49fbef7fdc", "start_char": 0, "end_char": 1364, "text_sha256": "e7118afd8c6055ed926ee24dbb7a07538f676163d605115ae0d32d49fbef7fdc"}
    experimental_model
    Human xCT expression and oxidative-stress response
    exposure
    hxCTb with 4F2hc; diethyl maleate challenge
    limitations
    Sodium independence belongs to this transporter; other cysteine-entry routes differ.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human transporter; Xenopus expression host
    plain_language
    The cells adjusted precursor uptake during the experimental challenge.
    primary_references
    [glutathione-p11406111] Human cystine/glutamate transporter: cDNA cloning and upregulation by oxidative stress in glioma cells. (2001). https://pubmed.ncbi.nlm.nih.gov/11406111/ DOI: 10.1016/s0005-2736(01)00338-8
    tissue_or_cell_type
    Oocyte membranes and human U87 glioma cells

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 749–760

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human xCT expression and oxidative-stress response · source_derived_draft · unverified_draft

    ### glutathione-xct-stress Diethyl maleate induced xCT expression and increased cystine uptake in U87 cells. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells adjusted precursor uptake during the experimental challenge. organism: Human transporter; Xenopus expression host tissue_or_cell_type: Oocyte membranes and human U87 glioma cells experimental_model: Human xCT expression and oxidative-stress response limitations: Sodium independence belongs to this transporter; other cysteine-entry routes differ. exposure: hxCTb with 4F2hc; diethyl maleate challenge evidence_span: {"source_cache": "artifacts/glutathione-research/11406111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7118afd8c6055ed926ee24dbb7a07538f676163d605115ae0d32d49fbef7fdc", "start_char": 0, "end_char": 1364, "text_sha256": "e7118afd8c6055ed926ee24dbb7a07538f676163d605115ae0d32d49fbef7fdc"} [glutathione-p11406111] Human cystine/glutamate transporter: cDNA cloning and upregulation by oxidative stress in glioma cells. (2001). https://pubmed.ncbi.nlm.nih.gov/11406111/ DOI: 10.1016/s0005-2736(01)00338-8
    Complete structured claim and evidence

  2. Erastin inhibited cystine uptake through system xc-minus, weakening antioxidant defenses before iron-dependent oxidative death.

    Erastin → cystine uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"}
    experimental_model
    Chemical and genetic characterization of nonapoptotic cell death
    exposure
    Erastin and ferrostatin-1 experiments
    limitations
    Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Cancer-cell systems and rat brain slices
    plain_language
    The death pathway connected iron with the supply of material needed for glutathione.
    primary_references
    [iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042
    tissue_or_cell_type
    Cellular iron, cystine transport and oxidative injury

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 1239–1250

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical and genetic characterization of nonapoptotic cell death · source_derived_draft · unverified_draft

    ### iron-cystine-ferroptosis Erastin inhibited cystine uptake through system xc-minus, weakening antioxidant defenses before iron-dependent oxidative death. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The death pathway connected iron with the supply of material needed for glutathione. organism: Cancer-cell systems and rat brain slices tissue_or_cell_type: Cellular iron, cystine transport and oxidative injury experimental_model: Chemical and genetic characterization of nonapoptotic cell death limitations: Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure. exposure: Erastin and ferrostatin-1 experiments evidence_span: {"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"} [iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042
    Complete structured claim and evidence

  3. Activated human CD4/CD8 T lymphocytes upregulate xCT and cystine uptake after TCR stimulation.

    SLC7A11 → cystine uptake source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    Activated CD4 and CD8 T cells
    experimental_model
    TCR-stimulated human CD4/CD8 lymphocytes
    limitations
    Not universal basal uptake in resting cells or a selenium supplementation result.
    organism
    Homo sapiens

    Selenium: literature corrections and mechanism additions · lines 1300–1310

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · TCR-stimulated human CD4/CD8 lymphocytes · secondary_verified · secondary_verified

    ## activated-xct Activated T cells can import cystine; resting cells need separate treatment. Activated human CD4/CD8 T lymphocytes upregulate xCT and cystine uptake after TCR stimulation. Organism: Homo sapiens Cell type: Activated CD4 and CD8 T cells Experimental model: TCR-stimulated human CD4/CD8 lymphocytes Limitations: Not universal basal uptake in resting cells or a selenium supplementation result. Primary reference: [Fluorescence-based measurement of cystine uptake through xCT shows requirement for ROS detoxification in activated lymphocytes](https://pmc.ncbi.nlm.nih.gov/articles/PMC5065394/)
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Increased extracellular cysteine supported cellular uptake and glutathione synthesis, bypassing dependence on cystine transport in the studied cells.

    Cellular cysteine uptake → Cellular reduced-glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/9288403.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6a14c857d89c580ffe8866d7e5f06658dcc806429ae3a4b8ad4bd096f664a2e2", "start_char": 0, "end_char": 1497, "text_sha256": "6a14c857d89c580ffe8866d7e5f06658dcc806429ae3a4b8ad4bd096f664a2e2"}
    experimental_model
    Cell-culture thiol transport and glutathione experiments
    exposure
    Lipoic acid/DHLA treatment and extracellular thiol measurements
    limitations
    Cell-type and extracellular-substrate dependence; no demonstration of general methylation-vitamin depletion.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Human, rat and mouse cells as specified
    plain_language
    The cells could import ready-to-use cysteine instead of relying on cystine uptake.
    primary_references
    [ala-p9288403] Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization. (1997). https://pubmed.ncbi.nlm.nih.gov/9288403/ DOI: 10.1002/biof.5520060303
    tissue_or_cell_type
    Human lymphocytes, Jurkat cells and erythrocytes; rat C6 and mouse NB41A3 cells

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 806–817

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-culture thiol transport and glutathione experiments · source_derived_draft · unverified_draft

    ### ala-cysteine-gsh-route Increased extracellular cysteine supported cellular uptake and glutathione synthesis, bypassing dependence on cystine transport in the studied cells. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells could import ready-to-use cysteine instead of relying on cystine uptake. organism: Human, rat and mouse cells as specified tissue_or_cell_type: Human lymphocytes, Jurkat cells and erythrocytes; rat C6 and mouse NB41A3 cells experimental_model: Cell-culture thiol transport and glutathione experiments limitations: Cell-type and extracellular-substrate dependence; no demonstration of general methylation-vitamin depletion. exposure: Lipoic acid/DHLA treatment and extracellular thiol measurements evidence_span: {"source_cache": "artifacts/ala-research/9288403.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6a14c857d89c580ffe8866d7e5f06658dcc806429ae3a4b8ad4bd096f664a2e2", "start_char": 0, "end_char": 1497, "text_sha256": "6a14c857d89c580ffe8866d7e5f06658dcc806429ae3a4b8ad4bd096f664a2e2"} [ala-p9288403] Lipoic acid increases de novo synthesis of cellular glutathione by improving cystine utilization. (1997). https://pubmed.ncbi.nlm.nih.gov/9288403/ DOI: 10.1002/biof.5520060303
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards