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Homocysteine affects cardiomyocyte viability: concentration-dependent effects on reversible flip-flop, apoptosis and

Jessica A Sipkens1, Paul A J Krijnen, Christof Meischl

  • 1Department of Pathology, VU University Medical Centre, Room 0E46, De Boelelaan 1117, Amsterdam, 1081 HV, The Netherlands. j.sipkens@vumc.nl

Apoptosis : an International Journal on Programmed Cell Death
|April 19, 2007
PubMed

Insights

High homocysteine (Hcy) concentrations cause concentration-dependent damage to cardiomyocytes, leading to cell death. This research clarifies Hcy

Area of Science:

  • Cardiovascular Science
  • Cell Biology
  • Biochemistry

Background:

  • Hyperhomocysteinaemia (HHC) is a potential risk factor for cardiovascular diseases, including heart failure.
  • Limited research exists on the specific effects of homocysteine (Hcy) on cardiac cells.
  • This study investigates the direct impact of Hcy on cardiomyocytes.

Purpose of the Study:

  • To analyze the effects of varying homocysteine (Hcy) concentrations on isolated cardiomyocytes.
  • To identify the cellular mechanisms and mediators involved in Hcy-induced cardiotoxicity.

Main Methods:

  • H9c2 rat cardiomyoblast cells and adult rat cardiomyocytes were exposed to different concentrations of Hcy.
  • Cell viability assays were performed.
  • Intracellular mediators including NOX2, reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), and ATP concentrations were quantified.

Main Results:

  • Low Hcy concentrations increased mitochondrial membrane potential and ATP levels.
  • Intermediate Hcy concentrations caused reversible plasma membrane phospholipid changes without inducing apoptosis.
  • High Hcy concentrations led to apoptosis and necrosis, characterized by mitochondrial dysfunction, ATP depletion, NOX2 expression, ROS production, and increased S-adenosylhomocysteine.

Conclusions:

  • Homocysteine exerts concentration-dependent effects on cardiomyocytes.
  • Hcy can induce reversible membrane changes, apoptosis, and necrosis in cardiac cells.
  • These findings highlight the direct cardiotoxic potential of Hcy, particularly at higher concentrations.
Abstract

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