ABSTRACT
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150 12.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150 12.2 Immune system in fish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
12.2.1 Innate (nonspecific) immunity . . . . . . . . . . . . . . . . . . . . . . . 151 12.2.2 Acquired (specific) immunity . . . . . . . . . . . . . . . . . . . . . . . . 152
12.2.2.1 Immunological methods . . . . . . . . . . . . . . . . . . . . 152 12.3 Ascorbic acid and immune response . . . . . . . . . . . . . . . . . . . . . . . . . 153
12.3.1 Channel catfish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153 12.3.2 Salmonid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154 12.3.3 Other species . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
12.4 Ascorbic acid (AA) and disease resistance . . . . . . . . . . . . . . . . . . . . 156 12.4.1 Channel catfish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156 12.4.2 Salmonid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160 12.4.3 Other species . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160
12.5 Interaction between ascorbic acid and other nutrients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160
12.6 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162
Abstract Due to the lack of L-gulonolactone oxidase enzyme, most fish species are unable to synthesize vitamin C (ascorbic acid) in sufficient quantity to meet metabolic needs, and thus have a requirement for this vitamin. Deficiency symptoms reported are structural deformities, impaired collagen synthesis, decreased alkaline phosphatase activity, hemorrhages, anemia, low tissue levels of ascorbic acid, anorexia, growth retardation, poor feed efficiency, and delayed wound healing. The requirements of vitamin C by fish to prevent these deficiency signs ranged from 11 to about 100 mg/kg of diet. Vitamin C has also been shown to influence immunity and disease resistance in fish. The fish immune system consists of innate (natural) and acquired (specific) immune mechanisms as have been reported for terrestrial animals. Published information appears to indicate that a deficiency in ascorbic acid is immunosuppressive, and animals fed ascorbic acid-deficient diets are more susceptible to infectious diseases than those fed vitamin C-replete diets. However, evidence on the role of ascorbic acid in improving the immune response and disease resistance in fish is not consistent, although numerous studies have indicated that feeding fish ascorbic acid at levels higher than those required for normal growth and prevention of deficiency signs enhanced their immune response and resistance against bacterial infection. Without clear evidence on the beneficial effect of high levels of ascorbic acid on the immune response and disease resistance, feeding fish vitamin C at a level sufficient to meet their requirement for growth and prevention of deficiency signs is suggested.
