Aquat Toxicol. 2025 Dec 21;291:107690. doi: 10.1016/j.aquatox.2025.107690. Online ahead of print.
ABSTRACT
Aluminum (Al) is a widespread aquatic neurotoxic pollutant, yet its brain accumulation is seldom quantified in fish neurotoxicity studies. Here, we investigated the neurobehavioral and molecular consequences of acute waterborne Al exposure in adult zebrafish (n = 227). Fish were exposed for 96 h to 50 mg/L AlCl₃ at pH 5.0 and then transferred to clean water for a 7-day depuration period. Despite the absence of statistically significant Al accumulation in either brain or carcass, exposed animals exhibited consistent neurobehavioral impairments, including reduced non-associative learning (short-term habituation of the acoustic startle response), anxiety- and depression-like phenotypes (positive geotaxis and negative scototaxis), and increased aggressive-like behavior. All behavioral alterations were fully reversed after depuration, indicating a transient effect. Brain oxidative stress markers (catalase, superoxide dismutase, lipid peroxidation), neurotransmitter levels, and acetylcholinesterase activity remained largely unchanged, arguing against a direct, generalized disruption of brain biochemistry. In contrast, brain expression of appa, gfap, and cat was significantly upregulated immediately after exposure and returned to control levels after depuration, suggesting an early but reversible stress and glial response. Overall, these findings show that short-term acidic Al exposure can induce reversible cognitive and affective disturbances in zebrafish in the absence of detectable brain accumulation, highlighting the importance of transient molecular stress pathways in acute aluminum neurotoxicity.
PMID:41453237 | DOI:10.1016/j.aquatox.2025.107690
