Thesis (M.Ag.Sc. 1978) from the Department of Animal Physiology, University of Adelaide.

Thesis (M. Inst. Agrar.)(Animal Production)--University of Pretoria, 2006. / Includes summary. Includes bibliographical references. Available on the Internet via the World Wide Web.

The biological activity or availability or feedstuff selenium was determined by comparing the effectiveness of the feedstuff with that of dietary sodium selenite in preventing the incidence of exudative diathesis in the chick. The available selenium in ten wheat samples varied from 62 to 178 percent with a mean of 105 percent. The selenium availability in rapeseed meal ranged from 27 to 89 percent with a mean of 61 percent. Selenium metabolism in the chick was investigated by adding graded levels of sodium selenite to the basal selenium deficient diet and comparing the dietary selenium concentration to the selenium concentration in the tissues (l.e. Blood, liver, kidney, and muscle of the chicks). The selenium content in the tissues examined increased proportionately to an increase in dietary selenium supplementation from 0 to 0.2 ppm. Blood and liver selenium concentration remain relatively constant (a slightly increasing plateau) from 0.2 to 1.0 ppm of dietary selenium. Above 1.0 ppm dietary selenium, blood and liver selenium levels increase steadily. These results show that either blood or liver selenium levels represent the selenium status of the bird. A similar response in tissue selenium levels of the chick was observed when selenium was supplied either as sodium selenite Or a feedstuff (brewers yeast). Furthermore, selenium levels birds fed wheat diets were similar to those fed equivalent selenium (sodium selenite) supplied in the basal diet. / Land and Food Systems, Faculty of / Graduate

A series of three experiments were carried out in order to demonstrate an interaction between molybdenum and selenium in broilers. Trail I investigated the interaction of selenium (0, 0.2, 0.4, and 0.8 ppm) with various toxic and subtoxic dietary levels of molybdenum (0, 0.5, 100, and 330 ppm), supplemented to a wheat based diet to broilers from one to four weeks of age. Results indicated that at 300 ppm molybdenum, increasing selenium levels resulted in progressive decline in weight gain, compared to a non-significant decline across these selenium levels when no molybdenum was supplemented. At these levels of molybdenum, selenium appeared to be acting antagonistically with molybdenum. At lower molybdenum levels, selenium exerted no apparent effects on weight gain. Selenium at toxic levels responded different from selenium at subtoxic dietary levels over molybdenum levels. Trial II, used 480 broiler chicks, assigned in a randomized block (RB) experimental design and 12 treatment combinations of selenium and molybdenum. Although the overall interaction effect was non-significant for weeks 1 to 4 inclusive, there were some definite interaction trends. Results indicated that at either basal or 3 ppm Se over basal 100, 200, or 300 ppm Mo, a non-significant difference in weight gain and feed consumption occurred. Selenium and molybdenum appeared to be interacting reciprocally. At 6 ppm dietary supplementation of selenium, however, combining increasing levels of molybdenum appeared to result in an independent toxic effect on weight gain which was additive for the two mineral toxicities, and not interactive. Using 480 broilers chicks assigned to a 3 x 4x3x3 multifactorial arrangement of 12 treatments an experiment was performed to investigate the effect on weight gain and feed consumption upon feeding toxic levels of molybdenum and selenium. Selenium levies ranged from basal, to 6, 12, and 18 ppm and molybdenum levels from basal, 400, and 800 ppm. Treatments were arranged in a RB experimental design. Results indicated that combining toxic dietary levels of selenium and molybdenum resulted in a measurable interaction in birds based on weight gain to feed consumption from one to four weeks of the experimental period. As the toxic dietary levels of selenium increased from basal to 6, 12, and 18 ppm the adverse effect of molybdenum at basal, 400 and 800 ppm became progressively reduced. At 18 ppm selenium, weight gain and feed consumption were the same irrespective of whether basal, 400, 800 ppm Mo was supplemented to the diet. The presence of toxic levels of selenium appeared to either reduce toxicity of molybdenum, or induce an increased tolerance for increasingly toxic levels of molybdenum. The nature of the interaction between selenium and molybdenum is discussed. / Land and Food Systems, Faculty of / Graduate

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Experiments were conducted to examine the role of dietary selenium (Se) and changes in antioxidant capacity during DMBA-induced mammary carcinogenesis. Weanling rats were fed graded amounts of Se in an AIN-76 diet, modified to approximate the amount and type of dietary fat consumed in Canada. Animals fed 3-4 ppm Se had a reduced tumor incidence but there was evidence of chronic Se toxicity. Low Se did not elevate tumor incidence. Thus, supplemental dietary Se did not offer any protection in reducing the incidence of cancer when rats were fed a diet representative of North American intakes of fat. Blood GSHPx activity was elevated in rats that remained free of tumors (NT group) compared to animals that would eventually develop tumors (WT group). SOD activity was reduced in WT and NT rats, but appeared to be related to carcinogen administration. These differences were observed before tumor development and over a wide range of Se intakes. WT rats excreted more $ sp{75}$Se compared to both control and NT rats. These changes, however, were not reflected in elevated lipid peroxidation. Thus, one of the protective mechanisms during carcinogenesis may be the capacity of the animal to elevate GSHPx activity.