Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex

  • Authors:
    • Leopold J. Anghileri
    • Emilio Mayayo
    • Jose L. Domingo
    • Pierre Thouvenot
  • View Affiliations

  • Published online on: January 1, 2002     https://doi.org/10.3892/or.9.1.61
  • Pages: 61-64
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Abstract

An in vivo comparative study of 45Ca-uptake and lipid peroxidation in tissues of mice treated with ATP complex of iron and sodium salt of ATP shows that only the iron complex produces a sustained increase of intracellular calcium on the organs susceptibles to develop lymphomas. A paralled study of 59Fe-uptake from 59Fe-iron complex of ATP presents a coincidental increase of iron uptake in those organs. To prove the involvement of the calcium homeostasis change in lymphoma-induction we have studied it with the lanthanum complex of ATP. Lanthanum is a well known cellular calcium entry modifier. Based on the results, the increased and sustained entry of extracellular calcium ion appears as the cause of lymphoma-induction by the iron complex. The effects of the calcium-overload in proliferation and neoplastic transformation of lymphocytes, as well as in reducing the immuno-response induced by thymus is discussed.

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January-February 2002
Volume 9 Issue 1

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Anghileri LJ, Mayayo E, Domingo JL and Thouvenot P: Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex. Oncol Rep 9: 61-64, 2002
APA
Anghileri, L.J., Mayayo, E., Domingo, J.L., & Thouvenot, P. (2002). Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex. Oncology Reports, 9, 61-64. https://doi.org/10.3892/or.9.1.61
MLA
Anghileri, L. J., Mayayo, E., Domingo, J. L., Thouvenot, P."Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex". Oncology Reports 9.1 (2002): 61-64.
Chicago
Anghileri, L. J., Mayayo, E., Domingo, J. L., Thouvenot, P."Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex". Oncology Reports 9, no. 1 (2002): 61-64. https://doi.org/10.3892/or.9.1.61