Association of Mitochondrial Dysfunction with Oxidative Stress and Immune Suppression in Blunt Snout Bream Megalobrama amblycephala Fed a High-Fat Diet

• Published in: Journal of aquatic animal health 2014-06, Vol.26 (2), p.100-112
• Main Authors: Lu, Kang-Le, Xu, Wei-Na, Liu, Wen-Bin, Wang, Li-Na, Zhang, Chun-Nuan, Li, Xiang-Fei
• Format: Article
• Language: English
• Subjects: adverse effects; Animal Feed - analysis; animal growth; Animal Nutritional Physiological Phenomena; Animals; apoptosis; complement; Cypriniformes; Dietary Fats - adverse effects; electron transport chain; fat intake; fatty liver; Fatty Liver - chemically induced; Fatty Liver - veterinary; fish; gene expression; gene expression regulation; glutathione; glycogen; hepatocytes; high fat diet; immune response; immune system; juveniles; leukocyte count; liver; Liver - drug effects; Liver - pathology; lysozyme; malondialdehyde; Megalobrama amblycephala; mitochondria; Mitochondria - metabolism; mortality; oxidative stress; Oxidative Stress - drug effects; sodium-potassium-exchanging ATPase; succinate dehydrogenase (quinone)
• ISSN: 1548-8667; 0899-7659; 1548-8667
• DOI: 10.1080/08997659.2014.893460

High-fat diets may have favorable effects on growth, partly based on protein sparing, but high-fat diets often lead to fatty liver (excessive fat deposition in the liver), which may be deleterious to fish growth and health. The goal of this study was therefore to investigate possible adverse effects and how they develop. Juvenile Blunt Snout Bream Megalobrama amblycephala (initial weight ± SE = 17.70 ± 0.10 g) were fed two diets (5% fat [control] or 15% fat). After 8 weeks, fish that were fed the 15% fat diet showed a high rate of mortality and poor growth. The histological results clearly showed that the high fat intake resulted in fat and glycogen accumulation and structural alterations of the hepatocytes, mitochondria, and nuclei. In the high-fat group, impairments of the mitochondria included mitochondrial swelling and the loss of cristae and matrix. Fish that were given the 15% fat diet exhibited low succinate dehydrogenase and Na ⁺,K ⁺-ATPase activities and increased cytochrome- c release from the mitochondria. Expression of genes for complex I and III subunits of the mitochondrial respiratory chain were down-regulated in fish that received the high-fat diet. Increases in malondialdehyde level and the ratio of oxidized glutathione to reduced glutathione suggested oxidative stress in the livers of fish from the high-fat diet group. Moreover, the lower leukocyte count, lysozyme and alternative complement activities, and globulin level in fish that received the high-fat diet indicated suppressive immune responses. Overall, the intake of excessive fat impaired mitochondrial bioenergetics and physiological functions. The dysfunction of the mitochondria subsequently mediated oxidative stress and hepatocyte apoptosis, which in turn led to the reduced efficacy of the immune system. Received July 15, 2013; accepted January 30, 2014.