Withdrawal effects following repeated ethanol exposure are prevented by N-acetylcysteine in zebrafish.

摘要: Abstract Alcohol abuse is a highly prevalent condition that substantially contributes to global morbidity and mortality. Most available pharmacological treatments offer little efficacy as relapse rates are high, due in part the symptoms experienced during abstinence. The roles of oxidative stress glutamatergic transmission alcohol withdrawal have been demonstrated several studies, suggesting restoration status function may represent new target prevent behavioral biochemical alterations observed withdrawal. A well-known antioxidant modulator, N-acetylcysteine (NAC), has shown promise treating variety psychiatric conditions, including substance use disorders, promising molecule management syndrome. Thus, aim this study was investigate whether NAC able expression induced by ethanol chronically exposed zebrafish. Animals were (1% v/v, 20 min) or control water, followed treatment with (1 mg/L, 10 min) water daily for 8 days; 24 h later, experimental animals submitted novel tank test (NTT). Ethanol decreased distance traveled increased number immobile episodes, indicating locomotor deficits; moreover, entries time spent top area, while increasing bottom anxiety-like behavior. also lipid peroxidation (TBARS) non-protein reduced sulfhydryl (NPSH) superoxide dismutase (SOD) catalase (CAT) activities. attenuated these deficits prevented manifestation behavior well damage following Given its favorable safety profile, additional clinical preclinical studies warranted unravel long-term effects context exact mechanisms involved. Nevertheless, our adds existing body evidence supporting evaluation disorders.