F. Boucher et al., ORAL SELENIUM SUPPLEMENTATION IN RATS REDUCES CARDIAC TOXICITY OF ADRIAMYCIN DURING ISCHEMIA AND REPERFUSION, Nutrition, 11(5), 1995, pp. 708-711
The aim of the present study was to assess whether an 8-wk oral seleni
um supplementation (standard food enriched with 2500 mu g Se/kg) in ra
ts might prevent the cardiotoxicity of adriamycin (ADR) treatment. ADR
was administered at a dose of 2.5 mg/kg body wt intraperitoneally twi
ce weekly for 3 wk. One week after the end of ADR treatment, rats (n =
10 per group) were killed and their hearts were perfused on a Langend
orff mode and subjected to a 30-min period of low-flow ischemia (resid
ual flow = 0.1 ml/min) followed by reperfusion (15 min). The results w
ere as follows: I) selenium supplementation significantly increased th
e activity of cardiac mitochondrial glutathione peroxidase (GPx) in AD
R-treated rats (control: 206 +/- 17.4 IU/g protein; Se: 277 +/- 24.5 I
U/g protein, p < 0.05); 2) selenium supplementation reduced myocardial
malondialdehyde content in ADR-treated rats (control: 1220 +/- 49.1 n
mol/g protein; Se: 1010 +/- 75.9 nmol/g protein; p < 0.05); and 3) ADR
treatment significantly increased the degree of reperfusion-induced s
tructural alterations to sarcomeres compared to untreated hearts. Agai
n, this phenomenon was abolished by selenium supplementation. In concl
usion, this study demonstrates that selenium supplementation is able t
o limit ADR cardiotoxicity in isolated rat hearts submitted to a seque
nce of ischemia/reperfusion.