Effect of NMDA Receptor Antagonist (APV)on the Toxicity Induced by Oxygen Radicals in Cultured Myocardial Cells.
10.11637/kjpa.1998.11.2.317
- Author:
Ock Kyu PARK
1
;
Jae Min OH
;
Jeong Joong KIM
;
Min Kyu CHOI
;
Seung Taeck PARK
;
Yeun Tai CHUNG
Author Information
1. Department of Internal Medicine, School of Medicine, Wonkwang University, Iksan 570 -749, Korea.
- Publication Type:Original Article
- Keywords:
Oxygen radical;
Cultured myocardial cell;
NMDA receptor antagonist
- MeSH:
6-Cyano-7-nitroquinoxaline-2,3-dione;
Animals;
Cell Survival;
Hypoxanthine;
Mice;
N-Methylaspartate*;
Oxygen*;
Reactive Oxygen Species*;
Xanthine Oxidase
- From:Korean Journal of Physical Anthropology
1998;11(2):317-325
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Toxic effect of oxygen radicals and cardioprotective effect of N -methyl -D -aspartate (NMDA) receptor antagonists against xanthine oxidase (XO) and hypoxanthine (HX)-induced cardiotoxicity were measured in order to elucidate the mechanism of cardiotoxicity on cultured mouse myocardial cells. MTT assay was performed after myocardial cells were cultured for 12 hours at various concentrations of XO/HX alone or with D -2 -amino -5 -phosphonovaleric acid (APV) or 6 - cyano -7 -nitroquinoxaline -2,3 -dione (CNQX). In this study, XO/HX was toxic in a time -and dose -dependent manners on cultured myocardial cells, and midcytotoxicity value 50 (MTT50) was at 30 mU/ml XO and 0.1 mM HX after myocardial cells were grown for 12 hours in media containing 1 ~50 mU/ml XO and 0.1 mM HX. When cultures were treated with 30 mU/ml XO and 0.1 mM HX flus 20 80 microM APV for 12 hours, cell viability was increased remarkably, while treatment with 30 mU/ml XO and 0.1 mM HX flus 10 ~50 microM CNQX did not show any protective effect against XO/HX -induced neurotoxicity. From the above results, it is suggested that oxygen radicals are toxic on cultured mouse myocardial cells by the decrease of cell viability, and NMDA receptor antagonists such as APV are very effective in the prevention of myocardial toxicity induced by oxygen radicals.
