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Liver ultrastructure during acute stress

M Salas, B Tuchweber, P Kourounakis

    Pathology, Research and Practice
    |January 1, 1980
    PubMed
    Summary
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    Acute stress triggers liver autophagy in rats, characterized by increased autophagic vacuoles and organelle degradation. This cellular process may represent an adaptive response to stress at the subcellular level.

    Area of Science:

    • Cell Biology
    • Stress Physiology
    • Histopathology

    Background:

    • Acute stressors induce significant physiological and morphological changes in organisms.
    • The liver plays a crucial role in metabolic regulation and response to stress.
    • Autophagy is a fundamental cellular process involving the degradation of cellular components.

    Purpose of the Study:

    • To investigate the ultrastructural, morphologic, and histochemical changes in rat livers under various acute stressors.
    • To determine the role of autophagy in the liver's response to acute stress.
    • To correlate liver changes with physiological stress markers.

    Main Methods:

    • Exposure of rats to eight different acute stressors for 48 hours.
    • Ultrastructural analysis using electron microscopy.

    Related Experiment Videos

  • Histochemical staining for glucose-6-phosphatase and acid phosphatase.
  • Measurement of plasma corticosterone levels and rectal temperature.

    • Main Results:

    • Stressors induced rough endoplasmic reticulum fragmentation, glycogen depletion, and mitochondrial enlargement in liver cells.
    • A significant increase in the number and size of autophagic vacuoles was observed.
    • Vacuolar membranes showed differential glucose-6-phosphatase reactivity, and vacuoles contained degraded organelles and acid phosphatase.
    • Increased plasma corticosterone and hypothermia were noted, with morphological changes correlating with hypothermia severity.

    Conclusions:

    • Acute stress induces significant autophagic activity in the rat liver.
    • Liver autophagy appears to be an adaptive subcellular response to acute stressors.
    • The observed changes suggest a coordinated cellular response to maintain homeostasis under stress.