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 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.

Diphenyl diselenide modulates splenic purinergic signaling in silver catfish fed diets contaminated with fumonisin B1: An attempt to improve immune and hemostatic responses.

The aim of this study was to determine whether purinergic signaling is a pathway associated with fumonisin B1 (FB1)-induced impairment of immune and hemostatic responses. We also determined whether dietary supplementation with diphenyl diselenide (Ph2Se2) 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 FB1-contaminated diets than in fish fed with a basal diet. Dietary supplementation with 3 mg Ph2Se2/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 FB1-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 FB1 intoxication. Supplementation with Ph2Se2 effectively modulated splenic enzymes associated with control of extracellular nucleotides (except ADP; that was partially modulated) and nucleosides, thereby limiting inflammatory and hemorrhagic processes.

Dietary addition of rutin impairs inflammatory response and protects muscle of silver catfish (Rhamdia quelen) from apoptosis and oxidative stress in Aeromonas hydrophila-induced infection.

This research aimed to assess the influence of dietary addition of rutin on inflammation, apoptosis and antioxidative responses in muscle of silver catfish (Rhamdia quelen) challenged with Aeromonas hydrophila (A. hydrophila). Fish were split into four groups as follows: control, 0.15% rutin, A. hydrophila, 0.15% rutin + A. hydrophila. After 2 weeks of feeding with standard or rutin diets, fish were challenged or not with A. hydrophila for 1 week. Rutin-added diet abrogates A. hydrophila induced-hemorrhage and inflammatory infiltration. It decreases A. hydrophila induced-apoptosis through decreasing the ratio of Bax to Bcl-2 and increasing phospho-Akt to Akt ratio. It diminishes the A. hydrophila induced-rise in nitric oxide and superoxide anion levels and reestablishes superoxide dismutase activity as well. Although such diet is unable to recover the levels of reduced glutathione (GSH), cysteine and glutamate cysteine ligase, which are depleted as a result of A. hydrophila infection, it diminishes the oxidized glutathione (GSSG) content, thus decreasing GSSG to GSH ratio. It increases the levels of cysteine residues of proteins and diminishes those of thiol-protein mixed disulfides, which were changed after A. hydrophila challenge. Finally, it reduces A. hydrophila induced-lipid peroxidation, markedly elevates ascorbic acid and thus reestablishes total antioxidant capacity, whose levels were decreased after A. hydrophila challenge. In conclusion, the dietary addition of rutin at 0.15% impairs A. hydrophila-induced inflammatory response, inhibits A. hydrophila-induced apoptosis and promotes cell survival. It also reduces the A. hydrophila-induced oxidative stress and stimulates the antioxidative responses in muscle of A. hydrophila-infected silver catfish.

Humic acid of commercial origin causes changes in gill morphology of silver catfish Rhamdia quelen exposed to acidic water: Response of silver catfish gills to low pH and humic acid.

The effect of dissolved organic carbon (DOC) against the burden of low pH was assessed in silver catfish Rhamdia quelen through the gills. A commercial humic acid (HA) was used as the source of DOC at 0 (control), 10, 25, and 50 mg/l. For each HA concentration, two pH levels were tested: 6.5 (control) and 5.5. After 40 days of exposure, the gills were removed and morphological variables were analyzed through light and scanning electronic microscopy. The low water pH caused a reduction in the length of filaments, number of lamellae, and gill respiratory surface area (GRSA) and an increase in chloride cells (CCs) number in the filament epithelium. When HA was added to the test water, GRSA increased and CCs proliferated in lamellae, suggesting ionic and respiratory disturbances. Scanning electronic microscopy revealed that CC morphometric variables, that is, apical area, fractional area, and density, were undisturbed by the pH reduction, but increased in the presence of HA. This study indicates that the commercial HA did not protect silver catfish against low pH stress. Instead, it caused changes that may affect vital processes such as ion regulation and ventilation and, consequently, reduce growth.