Cardiotoxicity associated with adriamycin (ADR) treatment limits the therapeutic efficiency of this drug aganist cancer. ADR causes morphological and functional alterations in mitochondrial, nuclear and fibrous protein structures in myoblasts. The study's aim was to determine whether the protection effect of selenium (Se) on ADR-induced cardiomyocyte toxicity.Rats were injected with (1) saline i.p for 21 days, (2) 2 mg/kg i.p ADR every alternate day (four times), (3) 0.15 mg/kg i.p Se for 21 days, (4) Se and ADR co-administration i.p. Left ventricular functions, ECG parameters and blood pressures were assessed by invasive techniques at the end of injection period. Mitochondrial membran potential (MMP, Cambrex Kit), ATP level (Cayman Kit ) and cytosolic thioredoxin reductase activity (TrxR, Cayman Kit) were determined. Cytosolic, intramitochondrial and plasma total antioxidant (TAS) and oxidant statuses (TAS) were measured with Erol's method.

Left ventricular data demonstrate a decrease in left ventricular systolic pressure (LVSP), left ventricular developed pressure (LVDP), and an increase in left ventricular end diastolic pressure (LVeDP) in ADR treated animals, compared to the control and Se groups. ADR increased ST interval and decreased systolic blood pressure, compared to the control and Se groups. ADR decreased membran potential and ATP level in myocite mitochondria. TrxR decreased in ADR group, compared to Se group. Cytosolic and mitochondrial TAS decreased and mitochondrial and plasma TOS increased in ADR group, compared to the control. ECG, blood pressure and left ventricular function changes by ADR recovered to control levels with co-administration Se with ADR. Se improved MMP and ATP level by decreasing oxidant and increasing antioxidant statues.

These data suggest that selenium reduces oxidative stress, prevents mitochondrial damage and protects cardiac myocytes against ADR toxicity.