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Related Experiment Videos

Hypothalamic digoxin mediated model for oncogenesis.

R K Kurup1, R Nair, P A Kurup

  • 1Dept. of Neurology, Medical College Hospital, Trivandrum, Kerala, India.

Journal of Experimental & Clinical Cancer Research : CR
|March 6, 2002
PubMed
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This study reveals altered isoprenoid metabolism, neurotransmitter patterns, and membrane integrity in brain and lymphoma cancers. These changes, including elevated digoxin and dolichol, contribute to oncogenesis through various cellular dysfunctions.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Neoplasms exhibit complex metabolic alterations.
  • The isoprenoid pathway and its metabolites play crucial roles in cellular processes.
  • Understanding these changes is vital for cancer research.

Purpose of the Study:

  • To investigate alterations in the isoprenoid pathway and related metabolites in CNS astrocytomas and non-Hodgkin's lymphoma.
  • To assess associated changes in tyrosine and tryptophan catabolites, glycoconjugate metabolism, RBC membrane composition, and free radical metabolism.
  • To elucidate the mechanisms linking these metabolic shifts to oncogenesis.

Main Methods:

  • Assessed isoprenoid pathway metabolites (digoxin, dolichol, ubiquinone).
  • Analyzed tyrosine and tryptophan catabolites, glycoconjugate metabolism, RBC membrane composition, and free radical metabolism.

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  • Measured enzyme activities, metabolite concentrations, and membrane component levels in cancer patients and controls.

    • Main Results:

    • Elevated plasma HMG CoA reductase, serum digoxin, and dolichol.
    • Reduced RBC membrane Na+-K+ ATPase activity, serum ubiquinone, and magnesium levels.
    • Altered tryptophan/tyrosine catabolites, increased glycosaminoglycans, elevated free radicals (MDA, hydroperoxides), and decreased scavenging enzymes.
    • Decreased HDL cholesterol, increased FFAs and triglycerides.

    Conclusions:

    • Elevated digoxin and altered membrane function contribute to oncogenesis via ion imbalance and transport defects.
    • Magnesium deficiency impacts microtubule function and chromosomal stability, promoting aneuploidy.
    • Metabolic shifts, including altered neurotransmitter patterns and glycoconjugate metabolism, drive neoplastic progression.
    • Mitochondrial dysfunction and increased oxidative stress, exacerbated by low ubiquinone, further promote cancer development.