Definition of streptozocin toxicity for primary lymphoidal tissues

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Updated: Nov 3, 2026

Isolation of Murine Lymph Node Stromal Cells
05:47

Isolation of Murine Lymph Node Stromal Cells

Published on: August 19, 2014

S R Wellhausen

    Diabetes
    |December 1, 1986
    PubMed

    Insights

    Streptozocin, but not alloxan, temporarily impacted DNA synthesis and lymphocyte levels in mouse lymphoid tissues. This study highlights streptozocin

    Area of Science:

    • Immunology
    • Endocrinology
    • Toxicology

    Background:

    • Hyperglycemia is a hallmark of diabetes mellitus.
    • Streptozocin and alloxan are diabetogenic agents used to induce hyperglycemia in animal models.
    • Primary lymphoidal tissues, including bone marrow and thymus, are crucial for immune cell development.

    Purpose of the Study:

    • To compare the effects of streptozocin and alloxan on primary lymphoidal tissues in BALB/c mice.
    • To investigate the impact of hyperglycemia induced by these agents on immune cell populations and function.

    Main Methods:

    • Induction of hyperglycemia in BALB/c mice using streptozocin or alloxan.
    • Assessment of in situ and in vitro DNA synthesis in bone marrow and thymus.
    • Evaluation of circulating lymphocyte and thymocyte populations.

    Main Results:

    • Streptozocin transiently inhibited DNA synthesis in bone marrow and thymus.
    • Streptozocin caused a temporary depletion of circulating lymphocytes and cortical thymocytes.
    • Alloxan did not exhibit these transient inhibitory effects on DNA synthesis or lymphocyte populations.
    • Streptozocin inhibited DNA synthesis in vitro in bone marrow and thymocyte cells.

    Conclusions:

    • Streptozocin has a more pronounced and transient effect on primary lymphoidal tissues compared to alloxan.
    • Even subdiabetogenic doses of streptozocin can lead to significant depletion of lymphocytes and thymocytes.
    • These findings are relevant for understanding the immunomodulatory effects of diabetogenic agents.

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