Vitamin E suspended progression of doxorubicin-induced heart damage (histopathology score 1.5 at 1.5 and 3 months) but offered no protection against doxorubicin plus cyclophosphamide.
Does vitamin E prevent cardiotoxicity induced by doxorubicin or doxorubicin with cyclophosphamide in mice?
Vitamin E may attenuate long-term myocardial damage from doxorubicin alone but is ineffective against the combination of doxorubicin and cyclophosphamide in a mouse model.
The aim of this study was to investigate the cardioprotective activity of vitamin E against doxorubicin alone and doxorubicin in combination with cyclophosphamide in mice. Female BalbC/NIH mice were treated with vitamin E (100 IU/kg, orally) 24 hr before single bolus doses of doxorubicin (10 mg/kg, intravenously), or doxorubicin and cyclophosphamide (150 mg/kg, intraperitoneally). Non-treated animals served as negative controls, while positive control groups received doxorubicin or doxorubicin and cyclophosphamide. For evaluation, serum enzyme activity of aspartate aminotransferase (AST), lactate dehidrogenase (LDH), alpha-hydroxybutirate dehydrogenase (alpha-HBDH), and creatine kinase (CK) at 48 hr and histopathology examination of the heart tissue (Billigham rules) at 1.5 and 3 months followed to treatments were used. In sera of mice treated with vitamin E prior to doxorubicin, the creatine kinase and % alpha-HBDH activity were significantly reduced, compared to positive control. Histopathology changes (scored as 1.5 at 1.5 and 3 months respectively) were not significant compared to negative control at both time points of examination. In animals which received vitamin E before doxorubicin and cyclophosphamide, none of the serum enzymes was significantly reduced compared to positive control, but non-significant increase in AST and creatine kinase activity was detected (3% and 16.57% respectively). The degree of myocardial damage was significantly higher compared to non-treated group (2.0 and 2.5 at 1.5 and 3 months respectively). Current results show that vitamin E in single oral dose failed to inhibit acute cardiotoxic activity of doxorubicin, but suspended further progression of the heart muscle damage over the time. On the contrary, vitamin E did not attain any cardioprotection against doxorubicin and cyclophosphamide in combination.
Bjelogrlić et al. (Tue,) conducted a other in Cardiotoxicity induced by doxorubicin and doxorubicin with cyclophosphamide. Vitamin E (d,l-α-Tocopherol) vs. Positive and negative controls was evaluated on Serum enzyme activity at 48 hr and histopathology examination of the heart tissue at 1.5 and 3 months. Vitamin E suspended progression of doxorubicin-induced heart damage (histopathology score 1.5 at 1.5 and 3 months) but offered no protection against doxorubicin plus cyclophosphamide.