Prevention of doxorubicin-induced cardiotoxicity by recombinant interleukin-1 in hamsters. Doxorubicin cardiotoxicity and interleukin-1.
The major factor contributing to doxorubicin (DXR)-induced cardiotoxicity is the insufficiency of antioxidant defense mechanisms. As a model of acute cardiotoxicity with DXR, ten-week-old golden hamsters were given DXR (5 mg/kg) intravenously, and the toxicity was investigated by monitoring ECG changes. Complete A-V block and cardiac arrest on the ECG were observed in DXR-treated hamsters. DXR-induced edema and fragmentation of myofibrils were observed by electron-micrograph. Pretreatment with interleukin-1 beta (10 or 1 microgram/body) 12 or 24 hrs before prevented these changes, but pretreatment with tumor necrosis factor alpha had no effect.
Yoshida
T
T
Department of Internal Medicine, Toyama Perefectural Central Hospital, Japan.
Okumura
H
H
Kaya
H
H
Okabe
Y
Y
Matano
S
S
Ohtake
S
S
Nakamura
S
S
Matsuda
T
T
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000517:prevention & control; D006224:Cricetinae; D004317:Doxorubicin / Q000633:toxicity*; D004562:Electrocardiography / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006327:Heart Block / Q000139:chemically induced / Q000517:prevention & control; D006331:Heart Diseases / Q000139:chemically induced* / Q000517:prevention & control*; D007375:Interleukin-1 / Q000627:therapeutic use*; D008297:Male; D008647:Mesocricetus; D009206:Myocardium / Q000648:ultrastructure; D011994:Recombinant Proteins / Q000627:therapeutic use
D007375:Interleukin-1; D011994:Recombinant Proteins; D004317:Doxorubicin