Next Article in Journal
Isolation and Identification of Antitrypanosomal and Antimycobacterial Active Steroids from the Sponge Haliclona simulans
Previous Article in Journal
Antibacterial and Antiyeast Compounds from Marine-Derived Bacteria
Article Menu

Export Article

Open AccessArticle
Mar. Drugs 2014, 12(5), 2922-2936; doi:10.3390/md12052922

Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center (CMDC), Inje University, Busan 614-735, Korea
Department of Health Sciences and Technology, Graduate School of Inje University, Busan 614-735, Korea
Elyakov Pacific Institute of Bioorganic Chemistry, Far-Eastern Branch of the Russian Academy of Science, Prospect 100 let Vladivostoku, 159, Vladivostok 690022, Russia
Author to whom correspondence should be addressed.
Received: 27 March 2014 / Revised: 22 April 2014 / Accepted: 28 April 2014 / Published: 13 May 2014
View Full-Text   |   Download PDF [531 KB, uploaded 24 February 2015]   |  


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. View Full-Text
Keywords: hrome A; mitochondrial function; cardiotoxic drugs; SNP; tBHP; doxorubicin hrome A; mitochondrial function; cardiotoxic drugs; SNP; tBHP; doxorubicin

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Jeong, S.H.; Kim, H.K.; Song, I.-S.; Lee, S.J.; Ko, K.S.; Rhee, B.D.; Kim, N.; Mishchenko, N.P.; Fedoryev, S.A.; Stonik, V.A.; Han, J. Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs. Mar. Drugs 2014, 12, 2922-2936.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Mar. Drugs EISSN 1660-3397 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top