Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis

Am J Physiol. 1992 Sep;263(3 Pt 2):R734-7. doi: 10.1152/ajpregu.1992.263.3.R734.

Abstract

During the progression of Mg deficiency in a rodent model, we have observed dramatic increases in serum levels of inflammatory cytokines [interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha)] after 3 wk on a Mg-deficient diet. Sequential analyses of these cytokine changes in the serum of rats revealed an initial rise at day 12, followed by a major elevation in all three cytokine levels by day 21. Of greater interest was an early peak in the serum level of the neuropeptide substance P after only 5 days on the diet. This "neuronal" tachykinin is thought to be released from neural tissues, and it is known to stimulate production of certain cytokines, including IL-1, IL-6, and TNF-alpha. In addition, there was a concomitant increase in histamine levels, which may have resulted from stimulation and degranulation of mast cells by substance P. Thus we hypothesize that the release of substance P may be the earliest pathophysiological event leading to stimulation of the inflammatory cytokines, which may then stimulate the free radical mechanisms of injury previously confirmed by our work.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cytokines / blood
  • Cytokines / physiology*
  • Inflammation / etiology
  • Inflammation / metabolism
  • Inflammation / physiopathology*
  • Magnesium Deficiency / etiology
  • Magnesium Deficiency / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Models, Biological*
  • Nervous System Physiological Phenomena*
  • Rats
  • Rats, Sprague-Dawley
  • Substance P / blood
  • Time Factors

Substances

  • Cytokines
  • Substance P