Influence of Dietary Astaxanthin on the Hepatic Oxidative Stress Response Caused by Episodic Hyperoxia in Rainbow Trout.

Lidia Robaina,Sachi Kaushik,María Soledad Izquierdo,Stéphanie Fontagné-Dicharry,Vincent Véron,Laurence Larroquet,Carmen Tatiana Kalinowski,Stéphane Panserat

doi:10.3390/antiox8120626

Abstract

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.

Highlights

Farmed fish are continuously exposed to stressful conditions induced by physical, chemical, and biological factors such as crowding, handling, changes in diets, and water quality, leading to susceptibility to viral or bacterial infections
Based on the hypothesis that dietary AX provides physiological benefits in terms of antioxidant defense, the present study aims to evaluate the homeostatic and stress responses in the liver of this species fed either a control diet (CTRL) or an astaxanthin-supplemented diet (ASTA), and exposed to two environmental conditions, normoxia and episodic hyperoxia, as a stressor causing oxidative stress
The experimental diets differed in AX content as CTRL diet had no AX and the ASTA diet was supplemented with 100 mg of chemically synthesized AX per kilogram of feed, a dietary level considered safe for salmonids according to the European Food Safety Authority [22]

Summary

Introduction

Farmed fish are continuously exposed to stressful conditions induced by physical, chemical, and biological factors such as crowding, handling, changes in diets, and water quality, leading to susceptibility to viral or bacterial infections. The red coloration of AX is due to the extended chain of conjugated double-bonds at the center of its chemical structure. This chain, including 13 double bonds, is responsible for the potent antioxidant effect of AX, involved in neutralizing singlet oxygen, scavenging superoxide anions, and hydroxyl radicals [8]. It can effectively scavenge lipid radicals and destroy peroxide chain reactions to protect polyunsaturated fatty acids (PUFAs) and sensitive membranes [9]

Methods

Discussion

Conclusion