Molecular and Cellular Biochemistry

, Volume 110, Issue 2, pp 169–173

Magnesium-deficiency elevates circulating levels of inflammatory cytokines and endothelin

Authors

  • William B. Weglicki
    • Department of MedicineThe George Washington University Medical Center
    • Department of PhysiologyThe George Washington University Medical Center
  • Terry M. Phillips
    • Department of MedicineThe George Washington University Medical Center
    • Department of PhysiologyThe George Washington University Medical Center
  • Anthony M. Freedman
    • Department of MedicineThe George Washington University Medical Center
    • Department of PhysiologyThe George Washington University Medical Center
  • Marie M. Cassidy
    • Department of MedicineThe George Washington University Medical Center
    • Department of PhysiologyThe George Washington University Medical Center
  • Benjamin F. Dickens
    • Department of MedicineThe George Washington University Medical Center
    • Department of PhysiologyThe George Washington University Medical Center
Article

DOI: 10.1007/BF02454195

Cite this article as:
Weglicki, W.B., Phillips, T.M., Freedman, A.M. et al. Mol Cell Biochem (1992) 110: 169. doi:10.1007/BF02454195

Summary

We have developed two rodent models of diet-induced magnesium-deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions, the magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-α together with signigicantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with magnesium deficiency.

Key words

cardiomyopathyTNF-αIL-1IL-6free radical mechanisms

Copyright information

© Kluwer Academic Publishers 1992