Nitrofurantoin-induced cardiotoxicity presents a significant concern in clinical practices, necessitating exploration of potential protective therapeutic agents against cardiotoxicity. This study investigates the cardioprotective efficacy of Coenzyme Q10 (CoQ10) against nitrofurantoin-induced cardiac damage. For this purpose, rabbits were categorized into four groups: control group was mock-treated with distal water only (G1), another group was treated with nitrofurantoin alone (G2), a third group with CoQ10 alone (G3), and a fourth group was treated with nitrofurantoin plus CoQ10 (G4). Serum levels of oxidative stress markers (e.g. MDA), cardiac injury markers (CPK and troponin), inflammation markers (e.g. CRP), and thyroid function (e.g TSH) were assessed. Additionally, histological examination was performed post-H andE staining to for pathological lesions. The group G2 exhibited elevated levels of MDA (4.22 ± 0.16 mmol/L), CPK (317.40 ± 0.24 U/L), and troponin (1.19 ± 0.004 mg/dL), which collectively indicated oxidative stress and cardiac injury. In response to treatment with CoQ10, especially in groups G3 and G4, histopathological alterations in cardiac tissue were decreased significantly, including areas of necrosis and vacuolation. More specifically, light microscopy demonstrated a trend toward reduction in necrosis and vacuolation in liver tissue in animals in group G3 and G4 compared to animals in G2. Respectively, in conjunction with the results for groups with no differences in serum CRP levels (0. 24 ± 0. 003 mg/dL), the animals in G4 showed aortic subintimal vacuolation points towards a modulatory effect also observed with CoQ10. These results clearly conclude that CoQ10 can ameliorate all the drug-induced side effects in the cardiac muscles and also points the directions for the future research on the potential benefits of CoQ10 in clinical settings.
Keywords | Coenzyme Q10, Cardiotoxicity, Nitrofurantoin, Cardiac protection, Antioxidant therapy