An acute phase response does not elevate rat heart metallothionein levels, nor inhibit adriamycin toxicity.
An acute phase response, a group of adaptations to some types of stress, blocks injury in rodents due to hepatotoxins and agents generating arthritis-like inflammation. In contrast, this study found no protection against adriamycin-induced acute cardiotoxicity in rats. The acute phase response was initiated by turpentine-stimulated leg inflammation. Injury was assessed by survival, macroscopic signs of injury, and heart lipid peroxidation. Acute phase response produced the expected rises in the stress-responsive proteins: serum ceruloplasmin and liver metallothionein. However, cardiac metallothionein was unaffected. These results suggest that an acute phase response will not necessarily protect tissues where levels of stress-induced proteins are not raised.
DiSilvestro
R A
RA
Ohio State University, Columbus 43210, USA.
Joseph
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E
D000210:Acute-Phase Reaction / Q000378:metabolism*; D000818:Animals; D002570:Ceruloplasmin / Q000378:metabolism; D004317:Doxorubicin / Q000633:toxicity*; D006321:Heart / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008297:Male; D008668:Metallothionein / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014425:Turpentine
D004317:Doxorubicin; D008668:Metallothionein; D002570:Ceruloplasmin; D014425:Turpentine