Inositol Lipid Turnover, Ca2+ Mobilization, and Increased Ca2+ Influx in Heat-Stressed Cells

  • M. A. Stevenson
  • E. K. Farnum
  • G. M. Hahn
  • S. K. Calderwood


We have investigated membrane permeability to Ca2+ and Ca2+ levels in cells subjected to heat stress. Heat caused a large and rapid rise in intracellular free calcium (Ca2+ i) within 2 min at 45°C Effects on transmembrane Ca2+ influx were more gradual, requiring 30 min at 45°C before increases were observed. The early rise in Ca2+ i appeared to be due to release from internal Ca2+ stores. Changes in Ca2+ homeostasis were correlated with alterations in membrane phosphoinositide (PI) turnover. The early rise in Ca2+ i was preceded by rapid (30 sec) release of inositol triphosphate, a PI catabolite that mobilizes Ca2+ from internal pools. Increased Ca2+ influx was closely correlated with membrane accumulation of phosphatidic acid, a lipid catabolite of PI with Ca2+ ionophoretic properties. The results indicate that heat, acting at the membrane, precipitates a cascade of interacting lipid and ionic changes that may be involved in the mediation of thermal injury.


PC12 Cell Heat Stress Intracellular Free Calcium Early Rise Inositol Triphosphate 
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Copyright information

© Plenum Press, New York 1987

Authors and Affiliations

  • M. A. Stevenson
    • 1
    • 2
  • E. K. Farnum
    • 1
    • 3
  • G. M. Hahn
    • 4
  • S. K. Calderwood
    • 1
  1. 1.Joint Center for Radiation TherapyDana Farber Cancer Institute Harvard Medical SchoolBostonUSA
  2. 2.Department of MedicineMassachussetts General HospitalBostonUSA
  3. 3.George Washington University Medical SchoolUSA
  4. 4.Cancer Biology Research LaboratoryStanford UniversityStanfordUSA

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