N-acetylcysteine provided substantial histological protection against doxorubicin-induced cardiac tissue damage in rats, despite not producing significant biochemical improvements.
Does N-acetylcysteine prevent doxorubicin-induced cardiotoxicity in rats?
N-acetylcysteine provides significant histological protection against doxorubicin-induced cardiac tissue damage in a rat model, highlighting its potential as a cardioprotective agent.
p-value: p=<0.005
Doxorubicin (DOX) is a widely used anthracycline antibiotic in the treatment of pediatric malignancies. However, its clinical application is significantly limited by its well-documented cardiotoxic side effects. The hypothesis of this study is that N-acetylcysteine (NAC), as an antioxidant agent, may reverse DOX-induced cardiotoxicity. Therefore, we aimed to evaluate the potential protective role of NAC against DOX-induced cardiotoxicity in rat heart tissue in this experimental study. Thirty rats were randomly divided into three groups (n = 10 each): control, DOX, and DOX + NAC. The control group received physiological saline via oral gavage at 0 and 24 h, followed by intraperitoneal saline at 48 h. The DOX group received saline at the same intervals, but received 20 mg/kg DOX intraperitoneally at 48 h. The treatment group received 140 mg/kg NAC orally at 0 and 24 h, followed by 20 mg/kg DOX intraperitoneally at 48 h. Compared to controls, the DOX group showed significantly increased malondialdehyde levels and decreased levels of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase (p < 0.05). In the NAC-treated group, these values were comparable to controls. Histologically, the DOX group exhibited edema, inflammation, vacuolization, hemorrhage, necrosis, and myofibrillar disorganization, while these alterations were largely absent in the NAC group (p < 0.005). In our study, NAC did not produce significant biochemical improvement in DOX-damaged heart tissue but provided substantial histological protection against DOX toxicity. These findings highlight NAC as a promising agent for reducing DOX-induced cardiac toxicity.
Tola et al. (Fri,) conducted a other in Doxorubicin-induced cardiotoxicity (n=30). N-acetylcysteine vs. Doxorubicin alone (20 mg/kg) and physiological saline was evaluated on Histological cardiac tissue damage (p=<0.005). N-acetylcysteine provided substantial histological protection against doxorubicin-induced cardiac tissue damage in rats, despite not producing significant biochemical improvements.