Search

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]

The aim of this study was to determine whether purinergic signaling is a pathway associated with fumonisin B 1 (FB 1)-induced impairment of immune and hemostatic responses. We also determined whether dietary supplementation with diphenyl diselenide (Ph 2 Se 2) prevents or reduces these effects. Splenic nucleoside triphosphate diphosphohydrolase (NTPDase) activity for adenosine triphosphate (ATP) and adenosine diphosphate (ADP) as substrates and total blood thrombocytes counts were significant lower in silver catfish fed with FB1-contaminated diets than in fish fed with a basal diet, while splenic adenosine deaminase (ADA) activity and metabolites of nitric oxide (NOx) levels were significant higher. Also, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were significant lower in silver catfish fed with FB 1 -contaminated diets than in fish fed with a basal diet. Dietary supplementation with 3 mg Ph 2 Se 2 /kg of feed effectively modulated splenic NTPDase (ATP as substrate), ADA, GPx and SOD activities, as well as NOx levels, and was partially effective in the modulation of spleen NTPDase activity (ADP as substrate) and total blood thrombocytes count. These data suggest that splenic purinergic signaling of silver catfish fed with FB 1 -contaminated diets generates a pro-inflammatory profile that contributes to impairment of immune and inflammatory responses, via reduction of splenic ATP hydrolysis followed possible ATP accumulation in the extracellular environment. Reduction of ADP hydrolysis associated with possible accumulation in the extracellular environment can be a pathophysiological response that restricts the hemorrhagic process elicited by FB 1 intoxication. Supplementation with Ph 2 Se 2 effectively modulated splenic enzymes associated with control of extracellular nucleotides (except ADP; that was partially modulated) and nucleosides, thereby limiting inflammatory and hemorrhagic processes. Unlabelled Image • Splenic NTPDase activity was significant lower in fish fed with FB 1 -contaminated diet. • Total thrombocytes counts were significant lower in fish fed with FB 1 -contaminated diet. • Diet with 3 mg Ph 2 Se 2 /kg of feed effectively modulated splenic NTPDase activity for ATP. • Ph 2 Se 2 effectively limited inflammatory and hemorrhagic processes. [ABSTRACT FROM AUTHOR]