Ameliorative Influence of Dietary Dates on Doxorubicin-Induced Cardiac Toxicity

Doxorubicin is a commonly used anticancer agent, which may cause cardiac toxicity. The present study designed to evaluate Phoenix dactylofera (dates) in doxorubicin (DXR) induced cardiac toxicity and cardiac remodeling in Wistar albino rats. The experimental rats procured, acclimatized and finally divided into five groups (n = 6). Group I served as normal controls, group II served as disease controls and groups 3, 4 & 5 served as therapeutic groups (Phoenix dactylofera 5%, 10%, and 15% respectively). Cardiac remodeling and toxicity in the rats were induced by administration of DXR (1.25 mg/kg i.p. in 16 divided doses/month). At the end of protocol, effect of Phoenix dactylofera on cardiac remodeling was evaluated by measuring parameters like haemodynamics, heart weight, anatomy, Troponin T, creatine phosphokinase (CPK), creatine phosphokinase-MB (CPK-MB), Lactate dehydrogenase (LDH), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), calcium ion Ca2+, sodium ion Na+, potassium ion K+, intracellular enzymes like Malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT). The disease control groups showed significantly elevated (p < 0.001) levels of troponin T, CPK, CPK-MB, LDH, MDA, and significantly reduced levels (p < 0.001) of GSH, SOD & CAT while the levels of SGPT, SGOT were increased less significantly (p < 0.01) as compared to therapeutic groups. Treatment with Phoenix dactylofera significantly (p < 0.01) reduced the increased levels of Troponin T, CPK, CPK-MB, LDH, SGOT, SGPT, MDA, GSH, SOD & CAT as well as restored Ca2+, Na+, K+ levels to a normal value. Further, the histological studies of the cardiac tissues demonstrated that the normal architecture of the cardiac cells was restored in the animals fed with dietary Phoenix dactylofera as compared to disease controls. The findings show that the administration of Phoenix dactylofera has the potential to prevent the toxicity induced by doxorubicin in the experimental rats.