This study was carried out in an attempt to assess the pattern of cathepsin D variations induced by Doxorubicin (DXR) and to clarify the role possibly played by this endopeptidase in the onset of anthracyclines-induced cardiotoxicity. We evaluated the variations in both total and 'sedimentable' enzyme activity of cathepsin D in the heart of mice treated once a week for up to 8 weeks with DXR (4 mg/kg i.v.b.wt.) and sacrificed 12h, 3 and 6 days after 1, 4, 5 and 8 administrations. Our results show that significant but transitory changes in both total and sedimentable activity of cathepsin D occur after each administration and decline after prolonged treatments. These data do not suggest, but do not exclude, a direct involvement of cathepsin D in the onset of DXR-induced cardiotoxicity: these phenomena might in fact be merely secondary to an increased catabolic activity of cathepsin D following an enhanced metabolic turnover of mitochondrial and myofibrillar protein damaged by DXR. This finding seems however quite interesting because cathepsin D variations might represent one of the long looked for biochemical marker of anthracyclines cardiotoxicity.

Leto G., Tumminello F.M., Gebbia N., Farruggia P., & Rausa L. (1987). Cathepsin D: A possible biochemical marker for anthracycline cardiomyopathy. MEDICAL SCIENCE RESEARCH, 15(23), 1471-1472.

Cathepsin D: A possible biochemical marker for anthracycline cardiomyopathy

Leto G.
;
Tumminello F. M.;Gebbia N.;Rausa L.
1987

Abstract

This study was carried out in an attempt to assess the pattern of cathepsin D variations induced by Doxorubicin (DXR) and to clarify the role possibly played by this endopeptidase in the onset of anthracyclines-induced cardiotoxicity. We evaluated the variations in both total and 'sedimentable' enzyme activity of cathepsin D in the heart of mice treated once a week for up to 8 weeks with DXR (4 mg/kg i.v.b.wt.) and sacrificed 12h, 3 and 6 days after 1, 4, 5 and 8 administrations. Our results show that significant but transitory changes in both total and sedimentable activity of cathepsin D occur after each administration and decline after prolonged treatments. These data do not suggest, but do not exclude, a direct involvement of cathepsin D in the onset of DXR-induced cardiotoxicity: these phenomena might in fact be merely secondary to an increased catabolic activity of cathepsin D following an enhanced metabolic turnover of mitochondrial and myofibrillar protein damaged by DXR. This finding seems however quite interesting because cathepsin D variations might represent one of the long looked for biochemical marker of anthracyclines cardiotoxicity.
Leto G., Tumminello F.M., Gebbia N., Farruggia P., & Rausa L. (1987). Cathepsin D: A possible biochemical marker for anthracycline cardiomyopathy. MEDICAL SCIENCE RESEARCH, 15(23), 1471-1472.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10447/434985
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