scholarly journals Some effects of selenium deficiency on glutathione peroxidase (EC 1.11.1.9) activity and tissue pathology in rainbow trout (Salmo gairdneri)

1986 ◽  
Vol 55 (2) ◽  
pp. 305-311 ◽  
Author(s):  
J. G. Bell ◽  
B. J. S. Pirie ◽  
J. W. Adron ◽  
C. B. Cowey

1. Two duplicate groups of rainbow trout (Sulmo gairdneri; mean weight 27 g) were given diets of differing selenium content (deficient 0, 025 mg Se/kg; supplemented 1.022 mg Se/kg) for 30 weeks.2. There were no significant differences between treatments in weight gain but packed cell volume, liver vitamin E and liver and plasma Se concentrations were all significantly lower in the Se-deficient trout.3. Ataxia occurred in about 10% of the Se-deficient trout and histopathologies were evident in nerve cord (damage to axon sheath) and liver (loss of integrity in endoplasmic reticulum and mitochondria with appearance of increased vesiculation).4. Glutathione peroxidase (EC 1.11.1.9) activity was significantly reduced in liver and plasma of Se-deficient fish but there was no indication, from differential assay, of any non-Se-dependent glutathione peroxidase activity. Glutathione transferase (EC 2.5. I.18) activity was significantly increased in Se-deficient trout.

1986 ◽  
Vol 56 (2) ◽  
pp. 421-428 ◽  
Author(s):  
J. G. Bell ◽  
J. W. Adron ◽  
C. B. Cowey

1. Duplicate groups of rainbow trout (Salmo gairdneri) were each given partially purified diets which were either adequate or depleted in selenium for 40 weeks.2. Although there was no significant difference in weight gain, liver Se concentration was significantly lower in fish given the deficient diet.3. Glutathione (GSH) peroxidase (EC 1. 11. 1. 9) activity was significantly reduced in liver of Se-deficient fish but a differential assay did not indicate the presence of a non-Se-dependent GSH peroxidase activity, although liver GSH S-transferase (EC 2. 5. 1. 18) was significantly increased.4. Perfusion of livers from trout given Se-adequate diets with t-butyl hydroperoxide (BuOOH) or hydrogen peroxide caused an increase in the rate of release of glutathione disulphide (GSSG) into the perfusate.5. Perfusion of livers from Se-deficient trout with BuOOH or H2O2 did not result in any change in rate of release of GSSG into the perfusate.6. These findings confirm the absence of any compensatory non-Se-dependent peroxidase activity in Se-depleted trout.


1984 ◽  
Vol 51 (3) ◽  
pp. 443-451 ◽  
Author(s):  
C. B. Cowey ◽  
Elizabeth Degener ◽  
A. G. J. Tacon ◽  
A. Youngson ◽  
J. G. Bell

1. Groups of rainbow trout (Salmo gairdneri) of approximate mean initial weight 8 g were grown in outdoor tanks over a 14-week period at water temperatures between 12° (start) and 6° (end). Four diets were used. Two contained non-oxidized fish oil (120 g/kg) with or without supplementary DL-α tocopheryl acetate and two contained moderately oxidized fish oil again with or without DL-α-tocopheryl acetate. The measured selenium content of the diets was 0.10 mg/kg.2. No significant differences occurred as a consequence of the use of moderately oxidized oil compared with the corresponding treatments using non-oxidized oil. Significant differences did occur between dietary treatments that contained supplementary DL-α-tocopheryl acetate and those that did not. These differences applied to weight gain, haematocrit, erythrocyte fragility, mortalities, liver and muscle tocopherol concentrations and lipid peroxidation of liver mitochondria in vitro. Liver glutathione peroxidase (EC 1.11.1.9) activity was unaffected by the dietary treatments used and the proportions of fatty acids in polar lipids of liver and muscle were little changed by the diets used. Severe muscle damage occurred in trout given diets lacking supplementary DL-α-tocopheryl acetate.3. Previous experiments carried out on rainbow trout at a constant water temperature of 15° (Hung et al. 1981; Cowey et al. 1981, 1983), using diets lacking supplementary vitamin E, did not lead to differences in weight gain, pathological changes or mortalities.4. Vitamin E requirement may increase as water temperature decreases; minimum dietary requirements for vitamin E measured at a constant water temperature of 15° may not be valid under practical conditions where water temperatures vary over the year.


1985 ◽  
Vol 53 (1) ◽  
pp. 149-157 ◽  
Author(s):  
J. G. Bell ◽  
C. B. Cowey ◽  
J. W. Adron ◽  
Aileen M. Shanks

1. Duplicate groups of rainbow trout (Salrno gairdnert) (mean weight 11 g) were given for 40 weeks one of four partially purified diets that were either adequate or low in selenium or vitamin E or both.2. Weight gains of trout given the dually deficient diet were significantly lower than those of trout given a complete diet or a diet deficient in Se. No mortalities occurred and the only pathology seen was exudative diathesis in the dually deficient trout.3. There was significant interaction between the two nutrients both with respect to packed cell volume and to malondialdehyde formation in the in vitro NADPH-dependent microsomal lipid peroxidation system.4. Tissue levels of vitamin E and Se decreased to very low levels in trout given diets lacking these nutrients. For plasma there was a significant effect of dietary vitamin E on Se concentration.5. Glutathione (GSH) peroxidase (EC 1. 1 1. 1.9) activity in liver and plasma was significantly lower in trout receiving low dietary Se but was independent of vitamin E intake. The ratios of hepatic GSH peroxidase activity measured with cumene hydroperoxide and hydrogen peroxide were the same for all treatments. This confirms the absence of a Se-independent GSH peroxidase activity in trout liver.6. Se deficiency did not lead to any compensatory increase in hepatic GSH transferase (EC 2. 5. 1. 18) activity; values were essentially the same in all treatments.7. Plasma pyruvate kinase (EC 2. 7. 1.40) activity increased significantly in the trout deficient in both nutrients. This was thought to be due to leakage of the enzyme from the muscle and may be indicative of incipient (subclinical) muscle damage.


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