Thesis (MSc (Veterinary Sciences))--University of Pretoria, 2001. / Includes bibliographical references.

The effect of a low-Cu diet supplied to gilts during pregnancy and early lactation on dams and their offspring was obtained in seven pairs of first littermate gilts. They were housed in stainless steel metabolism cages in a controlled environment and fed semi-purified diets containing either 2.13 or 12.25 ppm Cu from 30 days of gestation through two weeks of lactation. Feed intake was restricted to 2 kg/day during pregnancy and 4 kg/day in the first two weeks of lactation. Reproductive performance of gilts was measured. Balance studies were conducted at 30, 60 and 100 days of gestation. Mineral levels in the plasma of gilts and piglets, and in colostrum and milk were determined. The low-Cu diet did not affect (p $>$ 0.05) weight changes during pregnancy. The duration of parturition was shorter for low-Cu than for control gilts (3.19h vs 5.71h, p 0.05). Low-Cu gilts had lower plasma Cu in early- and mid-gestation and farrowed piglets with lower plasma Cu and higher plasma Zn concentrations (p 0.05). Plasma Cu and Fe levels of newborn piglets were lower than those of their dams (p 0.05). Low-Cu gilts had lower Cu and higher Zn content in colostrum and also lower Cu in milk than control gilts (p 0.05). Colostrum was richer in Cu and Zn than milk (p 0.05). Higher dry matter digestibility was observed in low-Cu gilts during early gestation (p 0.05). Compared to control gilts, the low-Cu gilts tended to have higher Cu and Zn retention which was achieved by reduction of fecal Cu and Zn excretion. Utilization of minerals appeared to increase as pregnancy progressed.

Thesis (M.S.)--Oregon State University, 2009. / Printout. Includes bibliographical references (leaves 76-79). Also available on the World Wide Web.

No description available.

Thesis (Ph. D.)--University of Missouri-Columbia, 2006. / "May 2006" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

Gas chromatography mass spectrometry (GCMS) and inductively coupled plasma mass spectrometry (ICPMS) were evaluated for the measurement of selenium (Se) and Se stable isotope ratios. GCMS and ICPMS were found to be accurate for quantitative Se analysis in biological matrices by isotope dilution using Se-78 and Se-76 as internal standards, respectively. A higher precision was obtained for ICPMS than GCMS enabling a smaller quantity of the tracer to be administered to subjects in labelling experiments. The isotopes of choice for metabolic tracers were Se-76 when sample analysis was by GCMS and Se-77 and Se-82 when analysis was by ICPMS. The influence of copper (Cu) on endogenous fecal Se excretion and true absorption of Se in nonlactating Holstein cows was examined by the use of Se stable isotopes as tracers. The method involved the application of conventional balance techniques in conjunction with isotopic enrichment of the body Se pools. Selenium in several tissues following oral and intravenous routes of isotope administration were evaluated as the precursors of endogenous fecal Se. Two cows fed a Se deficient diet (0.035 mg kg⁻¹) were administered 4 mg Se-76 orally, daily, for 5 d. After a 10-d equilibration period total collection of feces was made daily for two 5-d periods. The animals were then sacrificed and samples obtained from all major tissues and fluids. Se-7 6 enrichment (tracer/tracee mass percent, TTMP) in tissues was variable (< 0.56 - 13.4). However, enrichment was similar (9.8 - 12.9) in the tissues considered as potential contributors to endogenous fecal Se (serum, epithelium of the stomach, liver, bile, pancreas, small intestine and colon). Enrichment in serum and liver was used to calculate endogenous fecal Se. Apparent absorption of Se in the two cows was negative (-37 and -147 µg d⁻¹). Correction of apparent absorption for the fecal Se of endogenous origin gave a true Se absorption (% of intake) of 10 and 16%. The percentage of total fecal Se of endogenous origin was 23 and 36%. In two trials, 5 or 6 cows were assigned to one of two Cu-supplemented treatment diets: 0 mg kg⁻¹ or 17 mg kg⁻¹. The basal diet contained 0.19 mg Se kg⁻¹ and 13 mg Cu kg⁻¹. To each cow ~4.6 mg Se-77 and ~1.3 mg Se-82 were administered by oral and intravenous routes, respectively. After a 14-d equilibration period, total collection of feces and urine were made daily for two 5-d periods. Serum was collected on the first, third and fifth days of each period. Liver biopsies were taken 2 d following the completion of the balance periods. The estimates of endogenous fecal Se ( d⁻¹) from enrichment in the serum (256) and liver (235) following oral administration of the tracer and from enrichment in serum (241) following intravenous administration were not significantly different (P>0.05) but were higher than the estimate from the enrichment in liver (197) (P<0.05). No significant differences (P>0.05) were present when true absorption ( µg d⁻¹) was determined from enrichment in serum (290) or liver (268) following oral administration or from enrichment in serum (274) or liver (230) following intravenous administration. It was concluded the analysis of serum or liver with oral administration or the analysis of serum with intravenous administration of the tracer would provide reliable methods for estimation of endogenous fecal Se and true absorption. There was no effect of Cu on endogenous fecal Se excretion or true absorption of Se. Apparent and true absorption were 3.2 and 11%, respectively. Approximately 90% of the total Se excreted was in the feces, of which, 9.7% was of endogenous origin. The use of Se stable isotopes as metabolic tracers in dairy cattle provided a safe alternative to the use of radioactive tracers and enabled experiments requiring multi-isotopic enrichment to be performed. / Land and Food Systems, Faculty of / Graduate

No description available.

Two studies were conducted to determine how HDL cholesteryl ester and apoprotein catabolism might contribute to the observed hypercholesterolemia of copper-deficient rats. Weanling male Sprague-Dawley rats were divided into two dietary treatments; copper-adequate (control, 5-7 mg Cu/kg diet) and copper-deficient (0.6-0.8 mg Cu/kg diet). Deionized water and diet were provided ad libitum. Dietary copper deficiency resulted in enlarged intravascular pools of HDL cholesteryl esters and total protein. HDL were isolated from rats of both treatment groups, radiolabeled, and injected into animals of the respective groups. In Study I, HDL apoproteins were labeled by iodination, whereas HDL in Study II were doubly labeled by additionally incorporating into the particle core [³H]cholesteryl linoleyl ether, which served as a nondegradable analog of HDL cholesteryl ester. At specific time intervals up to 12 hours after injection, blood and tissue samples were removed and analyzed for radioactivity. Plasma disappearance curves indicated that HDL cholesteryl esters were preferentially catabolized 1.6-fold faster than HDL protein in controls and 2.5-fold faster in copper-deficient animals. Clearance of individual apoproteins did not occur at significantly different rates in either treatment group. Absolute mass removal of HDL cholesteryl ester and total protein from the plasma was significantly increased in copper-deficient rats. Virtually all of the increased removal of HDL cholesteryl ester was attributed to the liver, whereas most of the increased uptake of HDL protein was attributed to the bulk tissues and not the liver. Since previous studies indicate that copper deficiency may not result in increased cholesterol excretion, these data suggest that cholesteryl esters delivered to the liver of copper-deficient rats are possibly reassembled into new HDL particles at an increased rate. The observed hypercholesterolemia in this animal model, then, appears to be the result of an imbalance in the net flux of cholesterol between the tissues and the plasma.

No description available.

Two studies were designed to investigate the time course development of enlarged plasma volume and cholesterol pool size in copper (Cu)-deficient rats as well as influence of Cu deficiency on the lipid composition of lipoproteins. Rats were randomly assigned to three dietary Cu treatments (deficient, marginal, and adequate) in the Study I and two dietary Cu treatments (deficient and adequate) in Study II. Enlargement of plasma volume and cholesterol pool size were established prior to the increase in plasma cholesterol concentration. Cu concentration was decreased, whereas iron and zinc concentrations were increased in the organs of Cu-deficient and Cu-marginal rats. The plasma pool size of VLDL triglyceride was elevated 6-fold, protein and phospholipid were unaltered, and cholesterol was reduced 36%. The plasma pool size of lipid and protein components of HDL and LDL fractions were markedly elevated in Cu-deficient rats.