Russo S, Filippelli W, Ferraraccio F, Berrino L, Guarino V, Rossi F
Institute of Pharmacology and Toxicology, Faculty of Medicine and Surgery, II University of Naples, Italy.
J Med. 1994;25(1-2):65-89.
One of the most important factors that determine the therapeutic limits of doxorubicin (DXR), an anthracycline antibiotic, appears in acute and late cardiotoxicity. The aim of our investigations was to evaluate the effects of S-adenosylmethionine (SAMe), an important precursor of the organic sulfated compounds and a fundamental agent in physiologic transmethylation, on DXR-induced cardiotoxicity. For that purpose, normotensive Wistar rats were treated with DXR associated with or without SAMe. Pretreatment with SAMe significantly reduced DXR-induced electrocardiographic and morphologic changes, lethality, and body weight. The protective effect of SAMe may partly be due to its scavenger ability against free radicals and superoxides. In addition to its action as a fundamental precursor of the sulfated compounds, the principal agent in physiological transmethylations, and an increase of glutathione (GSH) synthesis.
