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

Abstract

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.

Keywords: Antioxidant system; Brain damage; Mycotoxins; Neurotoxicology; Selenium.