Oxidative stress markers and transporters expression in the heart of fructose-fed rats treated with the cardiotoxic antineoplasic doxorubicin

OGONOWSKI N; FELLET A; BALASZCZUK AM; KOUYOUMDZIAN NM; CHOI MR; RUKAVINA MIKUSIC NL; ROSON MI; CELUCH SM

Mar del Plata

Congreso; LXI Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

Sociedad Argentina de Investigación Clínica (SAIC)

&oxorubicin &1: clinical use as chemotherapeutic agent islimited due to the development of cardiomyopathies and heartfailure. 1ur interest is to study Yhether the cardiotoxicity of &1:could be increased in conditions Yith cardiovascular risM factors.+n this sense, Ye reported that in a model of metabolic syndromecaused by fructosefeeding F47 in rats, a single dose of &1:decreased the ejection and shortening fractions in the left ventricle,suggesting greater cardiotoxicity than in control C animals. $othF47 and &1: produce oxidative stress. /oreover, &1: changesthe expression of the plasma membrane transporter 2)2 Yhichextrudes &1: from cells. Also, a possible mechanism of its cardiotoxicityis the depletion of carnitine Yhich is uptaMen by 1CT0stransporters. The aim of this study Yas to analyze the effects of&1: on oxidative stress marMers and expression of 2)2 and1CT0s in cardiac tissue of C and F47 rats./ale Sprague&aYley rats receiving either tap Yater or YaterYith fructose during YeeMs Yere treated Yith &1: mg/Mg, ip, md or vehicle +SS n/group. Three days after injection,rats Yere sacrificed and left ventricles Yere excised to measureoxidative stress marMers and perform Yestern blot for 2)2 and1CT0//.$oth F47 and &1: enhanced T$A4S production Yith a significantincrease in the F47&1: group compared to C .v.vs .v. nmol/mg prot p.. There Yere not changes insuperoxide dismutase and catalase activities. The expression of2)2 in F47 Yas loYer than in C p.. &1: shoYed atendency to increase 2)2 expression, although F47&1: valuesremained loYer than C p.. Similar results Yere obtainedYith 1CT0s. +t is suggested that a minor efflux of &1: due toreduced expression of 2)2 and a possible depletion of carnitinerelated to decrease in 1CT0s expression could contribute to thegreater cardiotoxicity of &1: in F47 rats. Supported by C10+CET2+2