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Supplemental Microalgal DHA and Astaxanthin Affect Astaxanthin Metabolism and Redox Status of Juvenile Rainbow Trout.

ABSTRACT: Microalgal docosahexaenoic acid (DHA) and astaxanthin (AST) may substitute for fish oil and synthetic AST in aquafeeds. This study explored the effects and mechanisms of those substitutions on AST metabolism and redox status of rainbow trout fed plant protein meal (PM)- or fishmeal (FM)-based diets. Two parallel experiments (PM vs. FM) were performed with 612 juvenile rainbow trout for 16 weeks as a 2 × 3 factorial arrangement of treatments with two AST sources (synthetic (SA) vs. microalgal (AA), at 80 mg/kg) and three levels (0, 50, and 100%) of fish oil substitutions with DHA-rich microalgae. The fish oil substitutions exhibit main effects (p < 0.05) and/or interactive effects (p < 0.05) with the source of AST on AST deposition, malondialdehyde and glutathione concentrations, and mRNA levels and activities of major redox enzymes (glutathione reductase (GR), glutathione peroxidase (GPX), glutathione S-transferase (GST), and superoxide dismutase (SOD)) in the muscle and liver of trout fed both diet series. The AST source produced only differences in tissue AST deposition (p < 0.05) and number of metabolites. In conclusion, the substitutions of fish oil by the DHA-rich microalgae exerted more impacts than those of SA by AA on redox status and functional expression of antioxidant enzymes in the tissues of rainbow trout.

SUBMITTER: Wu K

PROVIDER: S-EPMC7823529 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:A 13-week feeding trial was carried out with juvenile rainbow trout to test two diets: a control diet without astaxanthin (AX) supplementation (CTRL diet), and a diet supplemented with 100 mg/kg of synthetic AX (ASTA diet). During the last week of the feeding trial, fish were exposed to episodic hyperoxia challenge for 8 consecutive hours per day. Episodic hyperoxia induced physiological stress responses characterized by a significant increase in plasma cortisol and hepatic glycogen and a decrease in plasma glucose levels. The decrease of plasma glucose and the increase of hepatic glycogen content due to episodic hyperoxia were emphasized with the ASTA diet. Hyperoxia led to an increase in thiobarbituric acid-reactive substances in the muscle, diminished by dietary AX supplementation in both liver and muscle. Muscle and liver AX were increased and decreased respectively after 7-day episodic hyperoxia, leading to an increase in flesh redness. This augment of muscle AX could not be attributed to AX mobilization, since plasma AX was not affected by hyperoxia. Moreover, hyperoxia decreased most of antioxidant enzyme activities in liver, whereas dietary AX supplementation specifically increased glutathione reductase activity. A higher mRNA level of hepatic glutathione reductase, thioredoxin reductase, and glutamate-cysteine ligase in trout fed the ASTA diet suggests the role of AX in glutathione and thioredoxin recycling and in de novo glutathione synthesis. Indeed, dietary AX supplementation improved the ratio between reduced and oxidized glutathione (GSH/GSSG) in liver. In addition, the ASTA diet up-regulated glucokinase and glucose-6-phosphate dehydrogenase mRNA level in the liver, signaling that dietary AX supplementation may also stimulate the oxidative phase of the pentose phosphate pathway that produces NADPH, which provides reducing power that counteracts oxidative stress. The present results provide a broader understanding of the mechanisms by which dietary AX is involved in the reduction of oxidative status.

Project description:We investigated the effects of chronic TCDD exposure on global gene expression in developing rainbow trout (Oncorhynchus mykiss). Juvenile rainbow trout (0.18M-BM-10.01g) were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100ppb, and ten fish were sampled and pooled from each group for microarray experiments at 28 days after initiation of the exposure. Gene expression analysis was performed using the Genomics Research on All Salmonids Project (cGRASP) 16K cDNA microarrays. TCDD-responsive whole body transcripts identified in the microarray experiments have putative functions involved in various biological processes including cellular process, metabolic process, biological regulation, and response to stimulus. In addition, TCDD caused leisons in multiple organ systems in juvenile rainbow, including skin, oropharynx, liver, gas bladder, intestine, pancreas, nose and kidney. Juvenile rainbow trout (0.18M-BM-10.01g) were fed Biodiet starter (Bio-Oregon) (4% body weight per day) with TCDD added at 0, 0.1, 1, 10 and 100 ppb. Fish were sampled after 28 days. Total RNA from individual fish was isolated using TRIzol reagent (Invitrogen). Total RNA of ten control trout were pooled as a common reference which were labeled with Cy3. Total RNA of ten fish of each treatment were labeled wih Cy5. cDNA were synthesized using SuperScript II Reverse Transcriptase (Invitrogen) (1 M-NM-<g pooled RNA per synthesis). Targets were labeled using the Array 900 Expression Array Detection kit (Genisphere) following the manufacture protocol. 1M-BM-5g RNA of pooled ten control fish were labled with Cy3 and 1M-BM-5g RNA of pooled ten TCDD-treated fish were labled with Cy5, then day-swap was performed. Two arrays were run for each comparison. Microarrays were scanned at 10 M-BM-5m resolution using a ScanArray Express (PerkinElmer Life Sciences, Inc, Boston, MA). The photomultiplier tube settings (PMT) for Cy3 and Cy5 were 70 and 65-66, respectively. TIFF images of arrays were generated with ScanArray Express software (PerkinElmer). Fluorescence intensity data for Cy3 and Cy5 channels were extracted from TIFF images using ImaGene 7.5 software (BioDiscovery Inc., El Segundo, CA). Background correction, data transformation (setting background corrected values < 0.01 to 0.01), Lowess normalization, and analysis (e.g. fold-change calculations) were performed using GeneSpring GX 7.3 (Agilent Technologies, Palo Alto, CA)

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Supplemental Microalgal DHA and Astaxanthin Affect Astaxanthin Metabolism and Redox Status of Juvenile Rainbow Trout.

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