Key result
Co-administration of the nitric oxide synthase inhibitor L-NAME with doxorubicin in rats significantly reduced plasma malondialdehyde levels compared to doxorubicin alone (p=0.03) and attenuated histopathological signs of cardiotoxicity.
Why the study?
Do nitric oxide synthase inhibitors reduce doxorubicin-induced cardiotoxicity in a rat model?
Do nitric oxide synthase inhibitors reduce doxorubicin-induced cardiotoxicity in a rat model?
p-value: p=0.03
In a rat model, the administration of nitric oxide synthase inhibitors alongside doxorubicin significantly attenuated doxorubicin-induced myocardial damage and lipid peroxidation.
Should not change practice; hypothesis-generating for nitric oxide inhibition in anthracycline cardiotoxicity.
Objective: We evaluated the myocardial damage in rats treated with doxorubicin (DOX) alone and in combination with nitric oxide synthase (nOS) inhibitors.
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Bahadır et al. (2013) studied Doxorubicin-induced cardiotoxicity (n=24). Nitric oxide synthase inhibitors (L-NAME and L-NIL) with doxorubicin vs. Doxorubicin alone (3 mg/kg weekly) was evaluated on Plasma malondialdehyde (MDA) level (p=0.03). Co-administration of the nitric oxide synthase inhibitor L-NAME with doxorubicin in rats significantly reduced plasma malondialdehyde levels compared to doxorubicin alone (p=0.03) and attenuated histopathological signs of cardiotoxicity.
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