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Study · In vitro (cells) · rabbit · 1994

5 results

5-aminoimidazole-4-carboxamide ribotide (AICAR) and its metabolites: metabolic and cytotoxic effects and accumulation during methotrexate treatment

Ha T, Baggott JE

The Journal of nutritional biochemistry1 Nov 1994Cited by 3 (Europe PMC)

DOI10.1016/0955-2863(94)90049-3 (opens in a new tab)PepBankPUB-98955939
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Activity measurement

    In human lymphoblast T cells, AICAR riboside potentiated methotrexate toxicity compared with methotrexate alone.

    In plain wordsIn cells, AICAR riboside increased methotrexate toxicity in human T cells compared with methotrexate alone.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMethotrexate cytotoxicity potentiation in T cells
    Study

    humann: not reported in source

    Human lymphoblast T cells
    Comparator
    Methotrexate without AICAR riboside
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and 5-aminoimidazole-4-carboxamide-riboside potentiated methotrexate toxicity only in T cells.
    1 context sentence
    Summary · context
    Methotrexote, at concentrations similar to blood levels of low-dose-treated patients (i.e., 10 and 20 nm), was cytotoxic to a culture of a human lymphoblast T cells but not to a culture of a human lymphoblast B cells.
  2. 02LabIn vitro (cells)Activity measurement

    In human lymphoblast B cells, AICAR riboside did not potentiate methotrexate toxicity, unlike in T cells.

    In plain wordsIn cells, AICAR riboside did not increase methotrexate toxicity in human B cells compared with methotrexate alone.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeMethotrexate cytotoxicity potentiation in B cells
    Study

    humann: not reported in source

    Human lymphoblast B cells
    Comparator
    Methotrexate without AICAR riboside
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    5-aminoimidazole-4-carboxamide ribotide accumulated in T cells but not B cells treated with methotrexate, and 5-aminoimidazole-4-carboxamide-riboside potentiated methotrexate toxicity only in T cells.
    1 context sentence
    Summary · context
    Methotrexote, at concentrations similar to blood levels of low-dose-treated patients (i.e., 10 and 20 nm), was cytotoxic to a culture of a human lymphoblast T cells but not to a culture of a human lymphoblast B cells.
  3. 03LabIn vitro (cells)Mechanism

    In cultured lymphoblasts, T-cell S-adenosyl homocysteine hydrolase was more sensitive to AICAR riboside inhibition than the B-cell enzyme.

    In plain wordsIn cells, AICAR riboside inhibited S-adenosyl homocysteine hydrolase more readily in T cells than in B cells.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseSensitivity of S-adenosyl homocysteine hydrolase to inhibition
    Study

    humann: not reported in source

    Cultured human lymphoblast T and B cells
    Comparator
    B cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The S-adenosyl homocysteine hydrolase activity of cultured T cells was more sensitive to inhibition by 5-aminoimidazole-4-carboxamide riboside in the medium when compared with B cells.
    1 context sentence
    Summary · context
    Methotrexote, at concentrations similar to blood levels of low-dose-treated patients (i.e., 10 and 20 nm), was cytotoxic to a culture of a human lymphoblast T cells but not to a culture of a human lymphoblast B cells.
  4. 04LabIn vitro (cell-free)Mechanism

    In enzyme tests using rheumatoid arthritis patient cells, AICAR riboside irreversibly inhibited S-adenosyl homocysteine hydrolase.

    In plain wordsIn lab tests, AICAR riboside irreversibly inhibited S-adenosyl homocysteine hydrolase from human blood cells.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIrreversible S-adenosyl homocysteine hydrolase inhibition
    Study

    humann: not reported in source

    Enzyme from peripheral blood mononuclear cells of rheumatoid arthritis patients
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    5-aminoimidazole-4-carboxamide ribotide and its riboside were found to be irreversible inhibitors of S-adenosyl homocysteine hydrolase (EC 3.3.1.1) using enzyme from peripheral blood mononuclear cells of rheumatoid arthritis patients and from rabbit erythrocytes.
  5. 05LabIn vitro (cell-free)Mechanism

    In enzyme tests using rabbit erythrocytes, AICAR riboside irreversibly inhibited S-adenosyl homocysteine hydrolase.

    In plain wordsIn lab tests using enzyme from rabbit red blood cells, AICAR riboside irreversibly inhibited S-adenosyl homocysteine hydrolase.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIrreversible S-adenosyl homocysteine hydrolase inhibition
    Study

    rabbitn: not reported in source

    Enzyme from rabbit erythrocytes
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    5-aminoimidazole-4-carboxamide ribotide and its riboside were found to be irreversible inhibitors of S-adenosyl homocysteine hydrolase (EC 3.3.1.1) using enzyme from peripheral blood mononuclear cells of rheumatoid arthritis patients and from rabbit erythrocytes.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

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