Graduate Thesis Or Dissertation
 

Vitamin E, selenium and tri-o-cresylphosphate interrelationships

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  • A two-part study was conducted to investigate some of the nutritional relationships between dietary tri-o-cresylphosphate (TOCP), a toxic stress material, and dietary vitamin E and selenium. In part one, growth rate of male weanling Long-Evans rats and day-old Japanese quail (Coturnix coturnix japonica) was used to determine the protective action of various levels of selenium and/or vitamin E in overcoming the growth depressant effect of dietary TOCP. Also, lipase activity was measured in pancreatic homogenates and intestinal contents of rats. In part two, experiments were conducted to determine the influence of TOCP on the capacity of dietary selenium (with glucose added in vitro) and dietary vitamin E to prevent in vitro red blood cell hemolysis. The addition of 0.2% TOCP to the torula yeast based diet low in vitamin E and selenium resulted in growth cessation of rats 12 to 20 days (depending on initial weight) before the control. Addition of 0.5, 1. 0, 2. 0 or 5.0 ppm selenium (Na₂SeO₃) resulted in a positive growth response; one ppm selenium was the most effective level. With supplemental vitamin E, 50, 100, 250, 500 or 1000 IU (dl-α-tocopherol) per kg of diet, positive growth responses resulted whereas the 10 IU level was ineffective. Supplementation of 0.0125% ethoxyquin (a synthetic antioxidant) produced no favorable growth response; dietary cystine (1%) initially improved the growth of TOCP-fed rats but did not prevent death. One ppm selenium with and without 500 IU vitamin E were the most effective treatments. Also, rats maintained on the basal diet plus 0. 2% TOCP for 33 days (cessation of growth occurred at 20 days) were supplemented with 1 ppm selenium + 100 IU dl-α tocopherol; the subsequent response in growth to selenium was immediate and marked in contrast to a lesser response to dl-a-tocopherol. In day-old Japanese quail fed a torula yeast diet low in vitamin E and selenium, growth ceased at nine days; 90% mortality had occurred by 17 days. Selenium (0. 5 ppm) supplementation prevented the cessation of growth and mortality. Quail supplemented with vitamin E (20 IU dl-α-tocopherol/kg of diet) grew poorly and 50% mortality occurred indicating a specific need for selenium. Quail fed 0. 10% TOCP responded poorly in growth when neither selenium nor vitamin E were supplemented to the diet. The addition of 0.5 ppm selenium greatly improved growth; supplementation of vitamin E alone was much less effective. Dietary TOCP did not appear to inhibit pancreatic lipase activity in rats in vivo or in vitro. An increase in activity was observed in rats supplemented with 0.5 and 1.0 ppm selenium. In contrast, activity was slightly depressed in pancreatic homogenates obtained from rats supplemented with dietary vitamin E. Activity of intestinal lipase followed the same apparent trend. Addition of TOCP to the diet of growing rats supplemented with 10 IU of dl-α-tocopherol/kg of diet increased the extent of dialuric acidinduced hemolysis of erythrocytes. Only an initial difference was evident with the higher level of vitamin E (50 IU dl-α-tocopherol/kg of diet) which was totally protective after 16 days. An adaptation to the low vitamin E intake apparently occurred because the percent hemolysis decreased following an initial rapid rise. Red cells from animals supplemented with selenium and low vitamin E autohemolyzed less when glucose was added to the incubation medium. Dietary TOCP (0. 2 %) completely blocked the effect of glucose in the 1 ppm selenium-supplemented cells; higher dietary selenium (5 ppm) only slightly reduced the inhibitory affect of TOCP. In contrast, TOCP interfered less with utilization of glucose in vitamin E supplemented erythrocytes. The results of this study indicate that TOCP is an antagonist of both selenium and vitamin E. The growth depression resulting from TOCP consumption is primarily the result of selenium antagonism.
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