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Gill longitudinal sections of O. niloticus fish stained with H & E. (a) Primary lamellae (Pr) and secondary lamellae (Sc) (normal). (b) Primary lamellae (Pr; 1 g vit.E). (c) Degeneration (D) in the secondary lamellae (2 g vit.E). (d) Hemorrhage (Hr) in the primary lamellae and separation (S) in the epithelial cells of the secondary lamellae (copperoxychloride). (e) Necrosis (N) and curling (Cr) in the epithelial cells of the secondary lamellae (1 g vit.E and copperoxychloride). (f) Separation (S) in the epithelial cells of the secondary lamellae (2 g vit.E and copperoxychloride). 

Gill longitudinal sections of O. niloticus fish stained with H & E. (a) Primary lamellae (Pr) and secondary lamellae (Sc) (normal). (b) Primary lamellae (Pr; 1 g vit.E). (c) Degeneration (D) in the secondary lamellae (2 g vit.E). (d) Hemorrhage (Hr) in the primary lamellae and separation (S) in the epithelial cells of the secondary lamellae (copperoxychloride). (e) Necrosis (N) and curling (Cr) in the epithelial cells of the secondary lamellae (1 g vit.E and copperoxychloride). (f) Separation (S) in the epithelial cells of the secondary lamellae (2 g vit.E and copperoxychloride). 

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Article
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A 2 × 3 factorial experiment was designed to study the effect of sublethal toxicity of technical grade copperoxychloride, dietary vitamin E, and their interaction on growth performance, some blood parameters, DNA fragmentation, and histopathological lesions of Nile tilapia (Oreochromis niloticus). The 96-h lethal concentration 50 (LC50) of copperox...

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Context 1
... abnormalities, with hepatocytes presenting a homogenous cytoplasm and a large central or subcentral spherical nucleus, and only some samples showed fatty de- generation ( Figure 1a). The hepatic parenchyma of fish fed a diet supplemented with 1 g vit.E showed degeneration (Figure 1b), while fish fed a diet supplemented with 2 g vit.E showed pyknosis (Figure 1c). Additionally, O. niloticus exposed to copperoxychlor- ide cleared the hemorrhage in their hepatic parenchyma (Figure 1d). However, the hep- atic parenchyma of fish exposed to copperoxychloride and fed 1 g vit.E suffered only from focal necrosis (Figure 1e). Finally, O. niloticus exposed to copperoxychloride and fed 2 g vit.E showed congestion in the blood sinusoid (Figure 1f ). Gill histology from control and exposed fish is briefly illustrated in Figure 2. The gill morphology of the control tilapia was similar to that of other teleost fish species (Wilson and Laurent 2002). In fish fed diet with vit.E and not treated with fungicide, the gill was made up of double rows of filaments (primary lamellae) from which lamellae (secondary lamellae) arise perpendicularly. The lamellae were lined by a squamous epithelium com- posed of pavement and non-differentiated cells. The gill obtained from fish fed diet supplemented with l and 2 g vitamin E showed normal appearance of gill primary and secondary lamellae. On the other hand, only some samples showed cell degeneration (Figure 2a,b,c), while fish exposed to copperoxychloride showed hemorrhage in the pri- mary lamellae and separation in the epithelial cells of the secondary lamellae (Figure 2d). However, fish exposed to copperoxychloride and fed 1 g vit.E suffered from necrosis and curling in the gill epithelial cells of the secondary lamellae (Figure 2e). Finally, fish exposed to copperoxychloride and fed 2 g vit.E showed separation in the epithelial cells of the secondary lamellae (Figure 2f ...
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... abnormalities, with hepatocytes presenting a homogenous cytoplasm and a large central or subcentral spherical nucleus, and only some samples showed fatty de- generation ( Figure 1a). The hepatic parenchyma of fish fed a diet supplemented with 1 g vit.E showed degeneration (Figure 1b), while fish fed a diet supplemented with 2 g vit.E showed pyknosis (Figure 1c). Additionally, O. niloticus exposed to copperoxychlor- ide cleared the hemorrhage in their hepatic parenchyma (Figure 1d). However, the hep- atic parenchyma of fish exposed to copperoxychloride and fed 1 g vit.E suffered only from focal necrosis (Figure 1e). Finally, O. niloticus exposed to copperoxychloride and fed 2 g vit.E showed congestion in the blood sinusoid (Figure 1f ). Gill histology from control and exposed fish is briefly illustrated in Figure 2. The gill morphology of the control tilapia was similar to that of other teleost fish species (Wilson and Laurent 2002). In fish fed diet with vit.E and not treated with fungicide, the gill was made up of double rows of filaments (primary lamellae) from which lamellae (secondary lamellae) arise perpendicularly. The lamellae were lined by a squamous epithelium com- posed of pavement and non-differentiated cells. The gill obtained from fish fed diet supplemented with l and 2 g vitamin E showed normal appearance of gill primary and secondary lamellae. On the other hand, only some samples showed cell degeneration (Figure 2a,b,c), while fish exposed to copperoxychloride showed hemorrhage in the pri- mary lamellae and separation in the epithelial cells of the secondary lamellae (Figure 2d). However, fish exposed to copperoxychloride and fed 1 g vit.E suffered from necrosis and curling in the gill epithelial cells of the secondary lamellae (Figure 2e). Finally, fish exposed to copperoxychloride and fed 2 g vit.E showed separation in the epithelial cells of the secondary lamellae (Figure 2f ...
Context 3
... abnormalities, with hepatocytes presenting a homogenous cytoplasm and a large central or subcentral spherical nucleus, and only some samples showed fatty de- generation ( Figure 1a). The hepatic parenchyma of fish fed a diet supplemented with 1 g vit.E showed degeneration (Figure 1b), while fish fed a diet supplemented with 2 g vit.E showed pyknosis (Figure 1c). Additionally, O. niloticus exposed to copperoxychlor- ide cleared the hemorrhage in their hepatic parenchyma (Figure 1d). However, the hep- atic parenchyma of fish exposed to copperoxychloride and fed 1 g vit.E suffered only from focal necrosis (Figure 1e). Finally, O. niloticus exposed to copperoxychloride and fed 2 g vit.E showed congestion in the blood sinusoid (Figure 1f ). Gill histology from control and exposed fish is briefly illustrated in Figure 2. The gill morphology of the control tilapia was similar to that of other teleost fish species (Wilson and Laurent 2002). In fish fed diet with vit.E and not treated with fungicide, the gill was made up of double rows of filaments (primary lamellae) from which lamellae (secondary lamellae) arise perpendicularly. The lamellae were lined by a squamous epithelium com- posed of pavement and non-differentiated cells. The gill obtained from fish fed diet supplemented with l and 2 g vitamin E showed normal appearance of gill primary and secondary lamellae. On the other hand, only some samples showed cell degeneration (Figure 2a,b,c), while fish exposed to copperoxychloride showed hemorrhage in the pri- mary lamellae and separation in the epithelial cells of the secondary lamellae (Figure 2d). However, fish exposed to copperoxychloride and fed 1 g vit.E suffered from necrosis and curling in the gill epithelial cells of the secondary lamellae (Figure 2e). Finally, fish exposed to copperoxychloride and fed 2 g vit.E showed separation in the epithelial cells of the secondary lamellae (Figure 2f ...
Context 4
... abnormalities, with hepatocytes presenting a homogenous cytoplasm and a large central or subcentral spherical nucleus, and only some samples showed fatty de- generation ( Figure 1a). The hepatic parenchyma of fish fed a diet supplemented with 1 g vit.E showed degeneration (Figure 1b), while fish fed a diet supplemented with 2 g vit.E showed pyknosis (Figure 1c). Additionally, O. niloticus exposed to copperoxychlor- ide cleared the hemorrhage in their hepatic parenchyma (Figure 1d). However, the hep- atic parenchyma of fish exposed to copperoxychloride and fed 1 g vit.E suffered only from focal necrosis (Figure 1e). Finally, O. niloticus exposed to copperoxychloride and fed 2 g vit.E showed congestion in the blood sinusoid (Figure 1f ). Gill histology from control and exposed fish is briefly illustrated in Figure 2. The gill morphology of the control tilapia was similar to that of other teleost fish species (Wilson and Laurent 2002). In fish fed diet with vit.E and not treated with fungicide, the gill was made up of double rows of filaments (primary lamellae) from which lamellae (secondary lamellae) arise perpendicularly. The lamellae were lined by a squamous epithelium com- posed of pavement and non-differentiated cells. The gill obtained from fish fed diet supplemented with l and 2 g vitamin E showed normal appearance of gill primary and secondary lamellae. On the other hand, only some samples showed cell degeneration (Figure 2a,b,c), while fish exposed to copperoxychloride showed hemorrhage in the pri- mary lamellae and separation in the epithelial cells of the secondary lamellae (Figure 2d). However, fish exposed to copperoxychloride and fed 1 g vit.E suffered from necrosis and curling in the gill epithelial cells of the secondary lamellae (Figure 2e). Finally, fish exposed to copperoxychloride and fed 2 g vit.E showed separation in the epithelial cells of the secondary lamellae (Figure 2f ...
Context 5
... abnormalities, with hepatocytes presenting a homogenous cytoplasm and a large central or subcentral spherical nucleus, and only some samples showed fatty de- generation ( Figure 1a). The hepatic parenchyma of fish fed a diet supplemented with 1 g vit.E showed degeneration (Figure 1b), while fish fed a diet supplemented with 2 g vit.E showed pyknosis (Figure 1c). Additionally, O. niloticus exposed to copperoxychlor- ide cleared the hemorrhage in their hepatic parenchyma (Figure 1d). However, the hep- atic parenchyma of fish exposed to copperoxychloride and fed 1 g vit.E suffered only from focal necrosis (Figure 1e). Finally, O. niloticus exposed to copperoxychloride and fed 2 g vit.E showed congestion in the blood sinusoid (Figure 1f ). Gill histology from control and exposed fish is briefly illustrated in Figure 2. The gill morphology of the control tilapia was similar to that of other teleost fish species (Wilson and Laurent 2002). In fish fed diet with vit.E and not treated with fungicide, the gill was made up of double rows of filaments (primary lamellae) from which lamellae (secondary lamellae) arise perpendicularly. The lamellae were lined by a squamous epithelium com- posed of pavement and non-differentiated cells. The gill obtained from fish fed diet supplemented with l and 2 g vitamin E showed normal appearance of gill primary and secondary lamellae. On the other hand, only some samples showed cell degeneration (Figure 2a,b,c), while fish exposed to copperoxychloride showed hemorrhage in the pri- mary lamellae and separation in the epithelial cells of the secondary lamellae (Figure 2d). However, fish exposed to copperoxychloride and fed 1 g vit.E suffered from necrosis and curling in the gill epithelial cells of the secondary lamellae (Figure 2e). Finally, fish exposed to copperoxychloride and fed 2 g vit.E showed separation in the epithelial cells of the secondary lamellae (Figure 2f ...

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Citations

... Selenium and vitamin E as antioxidants make the cell to act as a hunter of free radicals, thus preventing the autointoxication of immunological cells such as macrophages which represent the first processors of the information about the exotic bodies and providing maximum defense for the fish (Brake, 1997). Vitamin E (α-tocopherol) is one of the most significant antioxidant vitamins that acts as a fat-soluble antioxidant in biological membranes to protect lipids against peroxidative damages and maintaining the normal growth and metabolic functions of fish (Harabawy and Mosleh, 2014;Hassaan et al., 2014;Rengaraj and Hong, 2015). Mahmoud et al. (2012) have reported that, Vitamin E plays an essential role in elimination of mercury stress through antioxidant free radical mechanism. ...
... Ibrahim (2011) has reported that, vitamin E is closely related to the immunological system performance and has antioxidant properties, favoring integrity and fluidity of membranes; controls the oxidizing reactions of fatty acids, keeps cellular respiration and helping in avoiding the cell death. As well, vitamin E as a lipid soluble antioxidant, is playing a crucial role in protection of biological membranes, lipoproteins and lipid stores against oxidation (Mekkawy et al., 2013;Hassaan et al., 2014); it plays an important role in scavenging lipid peroxyl radicals which are the chain-carrying species and propagate lipid peroxidation ((El-Demerdash et al., 2004); and necessary to improvement and maintenance of fish immunity, normal resistance of erythrocytes to haemolysis (Halver, 2002;Hassaan et al., 2014). ...
... Ibrahim (2011) has reported that, vitamin E is closely related to the immunological system performance and has antioxidant properties, favoring integrity and fluidity of membranes; controls the oxidizing reactions of fatty acids, keeps cellular respiration and helping in avoiding the cell death. As well, vitamin E as a lipid soluble antioxidant, is playing a crucial role in protection of biological membranes, lipoproteins and lipid stores against oxidation (Mekkawy et al., 2013;Hassaan et al., 2014); it plays an important role in scavenging lipid peroxyl radicals which are the chain-carrying species and propagate lipid peroxidation ((El-Demerdash et al., 2004); and necessary to improvement and maintenance of fish immunity, normal resistance of erythrocytes to haemolysis (Halver, 2002;Hassaan et al., 2014). ...
... Genotoxicity of most toxic chemicals including metals comes from their ability to induce the production of a variety of highly reactive oxygen species (ROS) such as H 2 O 2 , O 2 À and OH À and electrophilic free-radical metabolites that interact with nucleophilic sites in DNA and causing breaks and other DNA damages (Waisberg et al., 2003;). Also, they able to form strong covalent bonds with DNA resulting in the formation of DNA adducts (pieces of DNA covalently bonded to a cancer-causing chemical) which prevent accurate replication and leads to occurrence of mutations (Hartwell et al., 2000; Igwilo et al., 2006). Many pollutants including metals act as clastogenic agents that cause chromosome breakage (formation of acentric fragments) or aneugenic agents (causes chromosome lagging); these clastogenic and aneugenic agents affect the spindle apparatus (Saleh and Alshehri, 2011 ). ...
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This study was carried out to investigate the genotoxic and cytotoxic potentials of sublethal concentration (5 mg L−1) of combined metals including Cd, Cu, Pb and Zn (1.25 mg L−1 of each) on erythrocytes of Nile tilapia, Oreochromis niloticus after exposure for five and seven days; and to evaluate the protective role of vitamin E alone and a combination of selenium (Se) with vitamins A, C and E which was added to the diet as antioxidants against the genotoxicity and cytotoxicity of these metals. This was accomplished by application of micronuclei (MN), binuclei (BN), nuclear abnormalities (NAs) assays in addition to morphological erythrocyte alteration (MAEs) assay. The results revealed that, exposure of O. niloticus to Cd, Cu, Pb and Zn induced the formation of nine genotoxic endpoints including MN, BN and seven patterns of NAs, kidney-shaped nuclei, blebbed nuclei, lobed nuclei, bilobed nuclei, notched nuclei, hook-shaped nuclei and vacuolated nuclei; and five patterns of morphological malformations were recorded as cytotoxic endpoints including echinocytes, acanthocytes, teardrop-like erythrocytes, microcytes and fused erythrocytes. Frequencies of these abnormalities were significantly different (p