Influence of selenium deficiency on the acute cardiotoxicity of adriamycin in rats

Abstract

The influence of selenium (Se) deficiency on the acute cardiotoxicity induced by the anticancer drug adriamycin (ADR) has been studied in rats by electrocardiography. Two categories were formed by feeding groups of rats a Se-supplemented and a Se-deficient diet. The supplemented animals were taken as normals. The two categories were treated with iv injections of saline solution containing ADR at doses of 0, 7.5, and 15 mg/kg body wt. The cardiac Se concentration and glutathione peroxidase (GSH-Px) activity in the Se-deficient groups were < 2% lower than in the normals. The normal groups showed significant widening of the SaT and QaT durations when given 15 mg/kg ADR. The Se-deficient groups exhibited a dose-dependent widening of the SaT and QaT duration at 7.5 and 15 mg/kg and narrowing of the PQ duration at 15 mg/kg ADR. No heart rate or QRS duration changes were detected in both categories. Our results suggest that an imbalance of the antioxidant system is associated with Se deficiency and that Se plays a role in preventing the cardiac functional disorder attributable to oxygen free radical formation induced by ADR.

Renal Antioxidant Enzymes and Fibrosis-Related Markers in the Rat Adriamycin Model

“…Increased concentrations of ROI under pathological conditions can be caused by higher synthesis of free radicals, by decreased breakdown of ROI via AOE or by both. Increased ROI production is capable of initiating lipid peroxidation [26]in the lipid-rich environment (in blood and renal cortex) induced by Adriamycin administration [this study, 9, 14, 27]. We and others have previously demonstrated that AOE and ROI contents may change considerably in diseased organs and particularly in kidney [28, 29, 30, 31].…”

“…ROI are reported to play a central role in Adriamycin toxicity [8, 25, 26]. Increased concentrations of ROI under pathological conditions can be caused by higher synthesis of free radicals, by decreased breakdown of ROI via AOE or by both.…”

Protecting against anthracycline‐induced myocardial damage: a review of the most promising strategies

“…Cancer patients have slightly lower mean selenium levels than do healthy controls (Faber et al , 1995). Several studies have found that selenium deficiency enhances doxorubicin cardiotoxicity in rats (Coudray et al , 1992; Matsuda et al , 1997). In other animal studies, selenium supplementation limited anthracycline‐induced cardiotoxicity by increasing the activity of cardiac mitochondrial GSHPx, reducing the myocardial malondialdehyde content, and abolishing the structural changes of sarcomeres induced by doxorubicin (Boucher et al , 1995).…”

Olive oil protects against chromosomal aberrations induced by doxorubicin in wistar rat bone marrow cells

“…Doxorubicin (DXR) is an important chemotherapeutic agent that induces cardiotoxicity, as well as chromosome aberrations. It is important to reduce its toxicity in normal cells, a goal that can be achieved by concurrent administration of free radical scavenging agents, such as antioxidants (Amara-Mokrane et al, 1996;Matsuda et al, 1997;Antunes and Takahashi, 1998). The present study was undertaken to investigate the modulatory effect of the simultaneous treatment with olive oil, a dietary antioxidant, on the clastogenic action of DXR in Wistar rat bone marrow cells.…”