Background: Alcohol consumption exerts toxic effects on the central nervous system, causing neurodegeneration and behavioral disorders. The neuroprotective potential of disulfiram (DSF), a widely used treatment for alcohol dependence, remains unclear. Thus, this study aimed to evaluate the effects of DSF on ethanol-induced neurodegeneration, behavioral impairments, and cardiovascular alterations. Materials and Methods: A total of 28 rats were randomly assigned to four groups: control, ethanol (EtOH), EtOH + DSF, and DSF. Ethanol (5 g/kg) was administered orally three times per week for 14 days. The EtOH + DSF group received ethanol plus DSF (100 mg/kg, intraperitoneally, i.p.) while the DSF group received DSF alone. Blood pressure was measured using tail-cuff plethysmography. Behavioral alterations were analyzed through the open field test (OFT), elevated plus maze (EPM), and forced swim test (FST). Brain tissues were examined histopathologically using hematoxylin–eosin and toluidine blue staining. Data were analyzed by analysis of variance (ANOVA) and the Kruskal–Wallis test. Results: In the EPM, no significant differences were found among the groups in open-arm activity or risk-assessment behaviors. The OFT showed a significant reduction in locomotor activity in the EtOH group (p < 0.0001). In the FST, ethanol increased immobility (p < 0.0001) and decreased the latency to immobility (p = 0.0014). Ethanol markedly lowered systolic, diastolic, and mean arterial pressures, whereas DSF elevated systolic and mean arterial pressures without affecting heart rate. DSF treatment affects systolic and mean arterial blood pressures. So for systolic blood pressure p = 0.002. For mean arterial blood pressure p = 0.024. Histological analysis revealed neuronal damage in the EtOH group, while DSF significantly reduced the number of degenerating neurons (p < 0.001). Conclusion: Ethanol exposure was associated with depression-like behavior, reduced locomotor activity, and hypotension. DSF treatment may improve behavioral outcomes, partially counteract ethanol-induced hypotension, and confer neuroprotective effects.
Koçak et al. (2026) studied this question.