WWW.WAS.ORG • WORLD AQUACULTURE • SEPTEMBER 2013 65 al. 2013a). One of the most noteworthy changes is the presence of large clear spaces within the cytoplasm, displacing other elements of the sarcoplasm. This alteration is the result of the massive influx of water, calcium and sodium as a consequence of the direct attack of ROS to the muscular cell membrane. The increase in Ca2+ was corroborated by the increased gene expression of µ-calpain (Betancor et al. 2013a) because intracellular Ca2+ concentration stimulates calpain activity. Calpains are calcium-dependent cytosolic enzymes capable of degrading proteins, although it has also been hypothesized that calpains may play a regulatory role in muscle growth (Watabe 2001). Moreover, the increase in sarcoplasmic Ca2+ may result in impairment of mitochondrial functionality and substantial swelling of the organelle with consequent outer membrane rupture (Kolkatowski and Vercesi 1999), which was also observed in transmission electronic microscopy sections. Another pathological alteration found, related to lipid oxidation, was the presence of numerous myelin figures (Figure 1B). In mammals, these structures have been correlated to endogenous material produced by intracellular lipid oxidation (DeGritz et al. 1994). Effect of Oxidative Stress on Other Tissues Oxidation causes adverse effects on diverse marine and freshwater species. Apart from negative effects on production parameters, such as reduced growth or increased mortalities (Wang et al. 2006), several pathological symptoms have been related to different sources of oxidative stress in adults and juveniles of different fish species (Table 2). Abnormal development of bone and skeletal tissues is a major issue in marine larviculture. Limited information is available to characterize specific alterations with factors related to rearing practices, such as nutrition or abiotic elements (Lall and Lewis-McCrea 2007). Different nutrients in first feeds play a central role in the appearance of skeletal malformation if they are not supplied during the larval phase (Cahu et al. 2003). However, information on the role of oxidized lipids and free radicals in the development of skeletal abnormalities in teleost fish is limited. Recent studies with seabream larvae show that high dietary levels of DHA induce a higher percentage of skeletal deformities. In these larvae, the value of TBARS is high, indicating peroxidative processes (Izquierdo et al. 2013). Similarly, seabass larvae fed high DHA content had an increased incidence of skeletal deformities (Betancor et al. 2012c) and muscular injuries. Vitamin E supplementation did not reduce the frequency of abnormalities observed in juvenile halibut fed oxidized diets (LewisMcCrea and Lall 2007) in seabream larvae fed high DHA rotifers (Izquierdo et al. 2013) or in seabass larvae (Betancor et al. 2012a,b, Betancor et al. 2013a). Therefore, dietary oxidative products can cause deficiencies of antioxidant nutrients, resulting in skeletal abnormalities. Liver is the other target organ of ROS, where ceroid pigment can appear in relation to the imbalance between anti- and prooxidants (Porta et al. 2002). Ceroid pigment within hepatocytes has been associated with numerous pathological conditions in which one of the main pathogenic factors is the deficiency of vitamin E. In the case of seabass larvae, only a mild ceroidosis was found (Betancor et al. 2011), indicating that muscle is the (CONTINUED ON PAGE 64) FIGURE 1. Seabass larvae fed diets with a 5 percent DHA and 300 mg of vitamin E (a) transversal thick section, toluidine blue staining and (b) ultrathin transversal section. (a) Edema (arrow) between red (RF) and white fibres (WF), vacuoles (V) inside some of the affected muscle and necrotic muscle fibers (*). (b) Hypercontracted muscle fibre (*) showing numerous myelin figures (black arrows) and disarrangement (white arrows).
RkJQdWJsaXNoZXIy MjExNDY=