Excessive intracellular zinc accumulation in cardiac and skeletal muscles of dystrophic hamsters

Alice J. Crawford, Syamal Bhattacharya

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Zinc has been reported to be important in protein synthesis, collagen crosslinking, membrane structure and function, cellular necrosis, muscle glycolysis, and cardiac dysfunction. As all these processes are affected by muscular dystrophy, we studied the Zn concentrations in the cardiac and skeletal muscles of 7-month-old male dystrophic hamsters with advanced hypertrophic cardiomyopathy. Age- and sex-matched normal hamsters served as controls. Calcium, magnesium, and copper concentrations were also measured in the dystrophic and normal tissues. Flame atomic absorption spectrophotometry was used for mineral quantitation of the nitric acid tissue extracts. Zn concentrations in the myocardium (P < 0.002), diaphragm (P < 0.005), and rectus femoris muscles (P < 0.001) were significantly elevated with concomitant elevations of Ca in dystrophic compared with normal hamsters. Although no appreciable changes in Cu or Mg concentrations were noted in the myocardium, slight depletions of Cu in the dystrophic diaphragm (P < 0.025) and Mg in the dystrophic rectus femoris (P < 0.05) were present. The intracellular Zn and Ca accumulations in the cardiac and skeletal muscles of dystrophic hamsters correlated with other dystrophic features such as increased rates of protein synthesis, significant myocardial enlargement, characteristic electrocardiographic and mechanophysiologic abnormalities, and classical histopathologic changes. We hypothesize that Zn2+ may be cotransported with Ca2+ across the cellular membrane or substituted for Ca2+ in certain pathways. These mechanisms may be affected by the high-energy ATP-pump and/or the sodium-potassium exchange system at the cellular level. Our observations suggest a possible pathogenetic involvement of Zn in muscular dystrophy which may be associated with an accelerated effort by the cellular system to repair the damaged cardiac and skeletal muscles.

Original languageEnglish (US)
Pages (from-to)265-276
Number of pages12
JournalExperimental Neurology
Volume95
Issue number2
DOIs
StatePublished - Jan 1 1987

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Cricetinae
Zinc
Myocardium
Skeletal Muscle
Muscular Dystrophies
Quadriceps Muscle
Diaphragm
Nitric Acid
Sodium-Potassium-Exchanging ATPase
Atomic Spectrophotometry
Tissue Extracts
Membranes
Hypertrophic Cardiomyopathy
Glycolysis
Cellular Structures
Magnesium
Minerals
Copper
Proteins
Necrosis

All Science Journal Classification (ASJC) codes

  • Neurology
  • Developmental Neuroscience

Cite this

Excessive intracellular zinc accumulation in cardiac and skeletal muscles of dystrophic hamsters. / Crawford, Alice J.; Bhattacharya, Syamal.

In: Experimental Neurology, Vol. 95, No. 2, 01.01.1987, p. 265-276.

Research output: Contribution to journalArticle

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