Diphenyl diselenide dietary supplementation protects against fumonisin B1-induced oxidative stress in brains of the silver catfish Rhamdia quelen.

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 B 1 (FB 1). The brain is an important target of FB 1 ; 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 (Ph 2 Se 2) in the brains of fish subjected to several environmental insults; nevertheless, its neuroprotective effects in fish fed with diets contaminated with FB 1 remain unknown. Therefore, the aim of this study was to evaluate whether oxidative damage may be a pathway associated with FB 1 -induced neurotoxicity, as well as to evaluate whether dietary supplementation with Ph 2 Se 2 prevents or reduces FB 1 -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 FB 1 -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, Ph 2 Se 2 prevented impairment of brain ACAP levels, as well as GPx and GST activities elicited by FB 1 -contaminated diets. These data suggest that dietary supplementation with 3 mg/kg Ph 2 Se 2 prevented FB 1 -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, Ph 2 Se 2 exerted its neuroprotective effects via ameliorative effects on the enzymatic and non-enzymatic antioxidant defense systems, and may be an approach to prevent FB 1 -induced brain oxidative stress; however, is not an alternative to prevent the impairment on performance caused by FB 1. Unlabelled Image • Fumonisin B 1 -contaminated diet induced brain damage. • Diphenyl diselenide prevented the occurrence of lipid and protein damage. • Diphenyl diselenide improved brain antioxidant system. • Diphenyl diselenide may be an approach to prevent FB 1 -induced brain oxidative stress. [ABSTRACT FROM AUTHOR]