Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Alcohol. 1993 Jul-Aug;10(4):285-90.

Cocaethylene toxicity in rat primary myocardial cell cultures.

Author information

  • 1College of Pharmacy, Division of Medicinal Chemistry and Pharmacodynamics, University of Oklahoma Health Sciences Center, Oklahoma City 73190.


Cocaethylene is a unique cocaine metabolite formed in the presence of ethanol by the liver. Neither acute nor chronic cardiotoxic effects of this metabolite have been investigated. The purpose of this study was to establish a time- and dose-dependent toxicity profile for cocaethylene in primary myocardial cell cultures established from 3-5-day-old Sprague-Dawley rats. Alterations in lactate dehydrogenase (LDH) release, lysosomal neutral red (NR) retention, thiobarbituric acid-reactive substances (TBARS), morphology, and beating activity were evaluated after treatment of cultures with cocaethylene doses ranging from 1.0 x 10(-3) to 1.0 x 10(-9) M from 1 to 24 h. LDH release was significantly elevated after 24 h only with those cultures exposed to the highest dose of cocaethylene (1.0 x 10(-3) M). The highest dose of cocaethylene also significantly depressed NR retention. While all doses of cocaethylene depressed contractile activity and altered cellular morphology by 24 h, there were no TBARS formed up to 15 h. Thus, both low and high doses of cocaethylene are injurious to the cellular integrity and contractility of myocardial cell cultures. Future studies are warranted to determine mechanisms of cocaethylene toxicity in this in vitro model of spontaneously contracting myocardial cells.

[PubMed - indexed for MEDLINE]

LinkOut - more resources

Full Text Sources

Molecular Biology Databases

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk