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Echinochrome A protects mitochondrial function in cardiomyocytes against cardiotoxic drugs.

Abstract
Echinochrome A (Ech A) is a naphthoquinoid pigment from sea urchins that possesses antioxidant, antimicrobial, anti-inflammatory and chelating abilities. Although Ech A is the active substance in the ophthalmic and cardiac drug Histochrome®, its underlying cardioprotective mechanisms are not well understood. In this study, we investigated the protective role of Ech A against toxic agents that induce death of rat cardiac myoblast H9c2 cells and isolated rat cardiomyocytes. We found that the cardiotoxic agents tert-Butyl hydroperoxide (tBHP, organic reactive oxygen species (ROS) inducer), sodium nitroprusside (SNP; anti-hypertension drug), and doxorubicin (anti-cancer drug) caused mitochondrial dysfunction such as increased ROS level and decreased mitochondrial membrane potential. Co-treatment with Ech A, however, prevented this decrease in membrane potential and increase in ROS level. Co-treatment of Ech A also reduced the effects of these cardiotoxic agents on mitochondrial oxidative phosphorylation and adenosine triphosphate level. These findings indicate the therapeutic potential of Ech A for reducing cardiotoxic agent-induced damage.
AuthorsSeung Hun Jeong, Hyoung Kyu Kim, In-Sung Song, Seon Joong Lee, Kyung Soo Ko, Byoung Doo Rhee, Nari Kim, Natalia P Mishchenko, Sergey A Fedoryev, Valentin A Stonik, Jin Han
JournalMarine drugs (Mar Drugs) Vol. 12 Issue 5 Pg. 2922-36 (May 13 2014) ISSN: 1660-3397 [Electronic] Switzerland
PMID24828295 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cardiotonic Agents
  • Cardiotoxins
  • Naphthoquinones
  • Reactive Oxygen Species
  • Adenosine Triphosphate
  • Mitogen-Activated Protein Kinases
  • echinochrome A
Topics
  • Adenosine Triphosphate (metabolism)
  • Animals
  • Cardiotonic Agents (pharmacology)
  • Cardiotoxins (antagonists & inhibitors, toxicity)
  • Cell Death (drug effects)
  • Membrane Potential, Mitochondrial (drug effects)
  • Mitochondria, Heart (drug effects)
  • Mitogen-Activated Protein Kinases (antagonists & inhibitors, metabolism)
  • Myocytes, Cardiac (drug effects)
  • Naphthoquinones (pharmacology)
  • Rats
  • Reactive Oxygen Species (metabolism)
  • Sea Urchins

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