Gold nanoparticles (GNP) have emerged as an alternative to biomaterials in biomedical applications. Research has clearly demonstrated the relative safety and low toxicity of these molecules. However, the possible neuroprotective effect of GNP on the central nervous system (CNS) and its relationship with neurological and psychiatric disorders remain unclear. Zebrafish is a reliable model to investigate the impact of ethanol (EtOH) consumption on the CNS, including reward signaling such as the cholinergic neurotransmission system. Here, we investigated whether cotreatment or pretreatment with GNP prevented EtOH-induced changes in acetylcholinesterase activity and oxidative stress in the brain of zebrafish. We exposed adult zebrafish to 2.5 mg·L⁻¹ GNP 1 h prior to EtOH (1% v/v) treatment for 1 h, and cotreated adult zebrafish simultaneously with both substances for 1 h. Pretreatment with GNP did not prevent EtOH-induced increase in the acetylcholinesterase activity, whereas cotreatment with 2.5 mg·L⁻¹ GNP and EtOH protected against this increase. The results also suggested similar protective effect on oxidative stress parameters in the zebrafish pretreated with GNP at 2.5 mg·L⁻¹. GNP significantly decreased the levels of thiobarbituric acid reactive species and dihydrodichlorofluorescein levels when cotreated with EtOH. GNP also prevented EtOH-induced increase in superoxide dismutase and catalase activities, suggesting a modulatory role of GNP in enzymatic antioxidant defenses. Our results showed that GNP was able to modulate the disruption of cholinergic and oxidative homeostasis in the brain of zebrafish. These findings indicate for the first time that zebrafish is an interesting perspective to investigate nanoparticles against disorders related to alcohol abuse.

金纳米粒子 (GNP) 已成为生物医学应用中生物材料的替代品。研究清楚地证明了这些分子的相对安全性和低毒性。然而，GNP 对中枢神经系统 (CNS) 可能的神经保护作用及其与神经和精神疾病的关系仍不清楚。斑马鱼是研究乙醇 (EtOH) 消耗对中枢神经系统影响的可靠模型，包括胆碱能神经传递系统等奖励信号。在这里，我们调查了 GNP 的共处理或预处理是否可以防止 EtOH 诱导的斑马鱼大脑中乙酰胆碱酯酶活性和氧化应激的变化。我们将成年斑马鱼暴露于 2.5 mg·L ^-1在 EtOH (1% v/v) 处理 1 小时之前的 GNP 1 小时，并同时与两种物质共同处理成年斑马鱼 1 小时。用 GNP 预处理并不能防止 EtOH 诱导的乙酰胆碱酯酶活性增加，而用 2.5 mg·L ^-1 GNP 和 EtOH 共同处理可以防止这种增加。结果还表明，在用 2.5 mg·L ^{-1的 GNP 预处理的斑马鱼中，对氧化应激参数有类似的保护作用。}. 当与 EtOH 共处理时，GNP 显着降低了硫代巴比妥酸活性物质的水平和二氢二氯荧光素的水平。GNP 还阻止了 EtOH 诱导的超氧化物歧化酶和过氧化氢酶活性的增加，这表明 GNP 在酶促抗氧化防御中具有调节作用。我们的研究结果表明，GNP 能够调节斑马鱼大脑中胆碱能和氧化稳态的破坏。这些发现首次表明斑马鱼是研究纳米粒子对抗与酒精滥用相关疾病的一个有趣的视角。