Ene Madalina, Savuca Alexandra, Ciobica Alin-Stelian, Jijie Roxana, Gurzu Irina Luciana, Hritcu Luminita Diana, Chelaru Ionut-Alexandru, Plavan Gabriel-Ionut, Nicoara Mircea Nicusor, Gurzu Bogdan
Department of Biology, Faculty of Biology, "Alexandru Ioan Cuza" University of Iasi, Carol I Avenue, 20A, 700505 Iasi, Romania.
Doctoral School of Geosciences, Faculty of Geography and Geology, "Alexandru Ioan Cuza" University of Iasi, Carol I Avenue, 20A, 700505 Iasi, Romania.
Toxics. 2025 Mar 8;13(3):193. doi: 10.3390/toxics13030193.
Zinc contamination in aquatic environments has become a growing concern due to its potential to bioaccumulate and induce neurotoxic effects in aquatic organisms. As an essential trace element, zinc plays a crucial role in various physiological processes, but excessive exposure can disrupt the gut-brain axis, leading to cognitive and behavioral impairments. Recent studies have suggested that probiotics may offer protective effects against environmental neurotoxins by modulating the gut microbiota and associated neurological functions. The zebrafish () has emerged as a valuable model organism for studying the biological mechanisms underlying neurotoxicity and potential therapeutic interventions. This study aimed to assess the effects of probiotics on cognitive impairments induced by zinc chloride (ZnCl) exposure in zebrafish. Specifically, zebrafish were exposed to ZnCl at concentrations of 0.5 mg/L and 1.0 mg/L for 96 h, followed by a 7-day post-exposure period to probiotics (, , ). ZnCl exposure at these concentrations is already known to induce behavioral and neuromotor deficits resembling Alzheimer's disease-like symptoms in zebrafish models, making it a suitable model for evaluating the neuroprotective potential of probiotics. Behavioral assessments including sociability tests along with short- and long-term memory evaluations were conducted using EthoVision XT 16 software. Memory tests demonstrated that ZnCl exposure impaired cognitive functions, while probiotic treatment did not significantly ameliorate these deficits. In the social behavior test, ZnCl at 0.5 mg/L resulted in a marked decrease in sociability, whereas exposure to 1.0 mg/L did not induce significant changes. However, post-exposure probiotic administration following ZnCl intoxication at 1.0 mg/L exhibited an anxiolytic effect on zebrafish. These findings suggest that probiotics may exhibit partial neurobehavioral benefits following zinc chloride-induced toxicity, particularly in mitigating anxiety-like behaviors rather than cognitive deficits. Further investigations are needed to elucidate the precise mechanisms by which probiotics interact with the gut-brain axis in the context of heavy metal neurotoxicity.
由于锌在水生环境中具有生物累积的潜力并能对水生生物产生神经毒性作用，其在水生环境中的污染问题日益受到关注。作为一种必需的微量元素，锌在各种生理过程中发挥着关键作用，但过度接触会破坏肠脑轴，导致认知和行为障碍。最近的研究表明，益生菌可能通过调节肠道微生物群和相关神经功能，对环境神经毒素提供保护作用。斑马鱼已成为研究神经毒性潜在生物学机制和潜在治疗干预措施的重要模式生物。本研究旨在评估益生菌对氯化锌（ZnCl）暴露诱导的斑马鱼认知障碍的影响。具体而言，将斑马鱼暴露于浓度为0.5毫克/升和1.0毫克/升的ZnCl中96小时，随后在暴露后给予益生菌（、、）7天。已知在这些浓度下暴露于ZnCl会在斑马鱼模型中诱导出类似于阿尔茨海默病样症状的行为和神经运动缺陷，这使其成为评估益生菌神经保护潜力的合适模型。使用EthoVision XT 16软件进行了包括社交能力测试以及短期和长期记忆评估在内的行为评估。记忆测试表明，ZnCl暴露会损害认知功能，而益生菌治疗并未显著改善这些缺陷。在社交行为测试中，0.5毫克/升的ZnCl导致社交能力显著下降，而暴露于1.0毫克/升则未引起显著变化。然而，在1.0毫克/升的ZnCl中毒后给予益生菌，对斑马鱼表现出抗焦虑作用。这些发现表明，在氯化锌诱导的毒性作用后，益生菌可能具有部分神经行为益处，特别是在减轻类似焦虑的行为而非认知缺陷方面。需要进一步研究以阐明在重金属神经毒性背景下益生菌与肠脑轴相互作用的确切机制。
