The trend toward using plant-based ingredients in aquafeeds has raised important concerns for aquaculture owing to the negative impacts of mycotoxins on fish health; with emphasis for contamination by fumonisin B₁ (FB₁). The brain is an important target of FB₁; however, study of the pathways linked to brain damage is limited to an analysis of histopathological alterations. Reports have demonstrated the protective effects of dietary supplementation with diphenyl diselenide (Ph₂Se₂) in the brains of fish subjected to several environmental insults; nevertheless, its neuroprotective effects in fish fed with diets contaminated with FB₁ remain unknown. Therefore, the aim of this study was to evaluate whether oxidative damage may be a pathway associated with FB₁-induced neurotoxicity, as well as to evaluate whether dietary supplementation with Ph₂Se₂ prevents or reduces FB₁-mediated brain oxidative damage in silver catfish. Brain reactive oxygen species (ROS), lipid peroxidation (LOOH) and protein carbonylation increased on day 30 post-feeding in animals that received FB₁-contaminated diets compared to the control group, while brain antioxidant capacity against peroxyl radicals (ACAP) levels and catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities were lower. Diphenyl diselenide dietary supplementation avoid increases in brain ROS levels, as well minimizing the augmentation of LOOH levels. Furthermore, Ph₂Se₂ prevented impairment of brain ACAP levels, as well as GPx and GST activities elicited by FB₁-contaminated diets. These data suggest that dietary supplementation with 3 mg/kg Ph₂Se₂ prevented FB₁-induced brain damage in silver catfish, and this protective effect occurred through avoided of excessive ROS production, as well as via prevention of brain lipid damage. Furthermore, Ph₂Se₂ exerted its neuroprotective effects via ameliorative effects on the enzymatic and non-enzymatic antioxidant defense systems, and may be an approach to prevent FB₁-induced brain oxidative stress; however, is not an alternative to prevent the impairment on performance caused by FB₁.

由于霉菌毒素对鱼类健康的负面影响，在水产饲料中使用植物性成分的趋势引起了水产养殖的重要关注。重点在于伏马菌素B ₁（FB ₁）的污染。大脑是FB ₁的重要目标; 然而，与脑损伤有关的途径的研究仅限于组织病理学改变的分析。有报告表明，膳食中添加二苯基二硒化物（Ph ₂ Se ₂）对遭受多种环境侵害的鱼类的大脑具有保护作用。但是，它对受FB ₁污染饮食的鱼类具有神经保护作用仍然未知。因此，本研究的目的是评估氧化损伤是否可能是与FB ₁诱导的神经毒性相关的途径，并评估膳食中添加Ph ₂ Se _2是否能预防或减少FB ₁介导的银中脑氧化损伤。鲶鱼。进食FB _1的动物进食后30天，大脑的活性氧（ROS），脂质过氧化（LOOH）和蛋白羰基化增加与对照组相比，饮食被污染，而大脑对过氧自由基（ACAP）和过氧化氢酶（CAT），谷胱甘肽过氧化物酶（GPx）和谷胱甘肽S-转移酶（GST）的抗氧化能力较低。二苯二硒化物的膳食补充剂可避免脑中ROS水平的升高，并尽量减少LOOH水平的升高。此外，Ph ₂ Se ₂防止了大脑ACAP水平的受损以及FB ₁污染饮食引起的GPx和GST活性降低。这些数据表明，饮食中添加3 mg / kg Ph ₂ Se _2可以预防FB ₁引起的silver鱼脑损伤，这种保护作用是通过避免过量的ROS产生以及防止脑脂质损伤而发生的。此外，Ph ₂ Se ₂通过改善酶和非酶抗氧化防御系统的作用发挥神经保护作用，可能是预防FB ₁诱导的脑氧化应激的一种方法。但是，这不是防止FB ₁导致性能下降的替代方法。