Abstract：
Environmental contamination by pharmaceuticals from industrial waste and anthropogenic activities poses adverse health effects on non-target organisms. We evaluated the neurobehavioral and biochemical responses accompanying exposure to ecological relevant concentrations of atenolol (0, 0.1, 1.0, and 10 µg/L) for seven uninterrupted days in adult zebrafish (Danio rerio). Atenolol-exposed fish exhibited anxiety-like behavior, characterized by significant bottom-dwelling with marked reduction in vertical exploration. Atenolol-exposed fish exhibited marked increase in the duration and frequency of aggressive events without altering their preference for conspecifics. Biochemical data using brain samples indicated that atenolol disrupted antioxidant enzyme activities and induced oxidative stress. Exposure to atenolol markedly decreased ATP and AMP hydrolysis without affecting ADP hydrolysis and acetylcholinesterase (AChE) activity. Atenolol significantly upregulated tryptophan hydroxylase 1 (tph1) mRNA expression but downregulated brain-derived neurotrophic factor (bdnf) mRNA. Collectively, waterborne atenolol elicits aggressive and anxiety-like responses in adult zebrafish, accompanied by oxidative stress, reduced nucleotide hydrolysis, altered tph1 and bdnf mRNA expression, which may impact the survival and health of fish in aquatic environment.
摘要：
工业废物和人为活动造成的药物环境污染对非目标生物造成了不利的健康影响。我们评估了成年斑马鱼（Daniorerio）连续7天暴露于生态相关浓度的阿替洛尔（0、0.1、1.0和10µg/L）的神经行为和生化反应。阿替洛尔暴露的鱼表现出焦虑样行为，其特征是底部居住明显，垂直勘探明显减少。暴露于阿替洛尔的鱼表现出侵袭性事件的持续时间和频率显着增加，而没有改变他们对物种的偏好。使用脑样本的生化数据表明，阿替洛尔破坏了抗氧化酶的活性并诱导了氧化应激。暴露于阿替洛尔可显着降低ATP和AMP的水解，而不影响ADP水解和乙酰胆碱酯酶（AChE）活性。阿替洛尔显著上调色氨酸羟化酶1（tph1）mRNA表达，但下调脑源性神经营养因子（bdnf）mRNA表达。总的来说，水性阿替洛尔在成年斑马鱼中引起侵袭性和焦虑样反应，伴随着氧化应激，还原核苷酸水解，改变tph1和bdnfmRNA表达，这可能会影响鱼类在水生环境中的生存和健康。
